LncRNA Meg3 Aggravates Renal Fibrosis Caused by Unilateral Ureteral Obstruction in Rats by Activating the Hedgehog Pathway.

BACKGROUND: The hedgehog signaling pathway exerts vital functions in regulating epithelial-to-mesenchymal transition (EMT) in renal interstitial fibrosis (RIF). It was reported that lncRNA-maternally expressed gene 3 (lncRNA Meg3) can regulate hepatic fibrosis by regulating the expression of smoothened (Smo) in the hedgehog signaling pathway. However, the specific role of lncRNA Meg3 in renal fibrosis resulting from unilateral ureteral obstruction (UUO) by regulating the hedgehog signaling pathway has not been reported. Hence, this research aimed to expound the effects of lncRNA Meg3 on renal fibrosis induced by UUO in rats via the hedgehog pathway. METHODS: Peripheral blood was collected from patients with chronic kidney disease (CKD, CKD group) and healthy volunteers (Normal group) at the same period. In addition, 6-week-old male Sprague-Dawley (SD) rats were divided to Sham, UUO, UUO+shRNA Negative control (shNC), and UUO+sh-Meg3 groups, and their kidney tissues and serum were gathered. Next, quantitative real-time polymerase chain reaction (qRT-PCR) was employed for detecting the lncRNA Meg3 expression level in the serum of patients and renal tissue of rats; kits for testing levels of blood urea nitrogen (BUN), creatinine (Cr), hydroxyproline (HYP), and 24-hour urine protein (24-up) in rats of each group; hematoxylin and eosin (HE) staining and Masson staining for observing kidney tissue and renal fibrosis level in rats; western blot for measuring levels of collagen type III (Col III), α-Smooth muscle actin (α-SMA), fibronectin, E-cadherin, sonic hedgehog (Shh), patched (Ptch) protein, smoothened (Smo) protein and glioma-associated oncogene homolog 1 (Gli1) protein expression. RESULTS: LncRNA Meg3 was highly expressed in CKD patients and UUO rats (p < 0.01). In contrast to the UUO+shNC group, knocking down lncRNA Meg3 improved renal injury, relieved pathological renal lesions, and reduced kidney fibrosis and related protein levels. It inhibited the hedgehog pathway in kidney tissues of UUO rats (p < 0.05 and p < 0.01). CONCLUSIONS: LncRNA Meg3 can aggravate UUO-induced rat renal fibrosis by activating the hedgehog pathway.

The aryl hydrocarbon receptor in immune regulation and autoimmune pathogenesis.

As a ligand-activated transcription factor, the aryl hydrocarbon receptor (AhR) is activated by structurally diverse ligands derived from the environment, diet, microorganisms, and metabolic activity. Recent studies have demonstrated that AhR plays a key role in modulating both innate and adaptive immune responses. Moreover, AhR regulates innate immune and lymphoid cell differentiation and function, which is involved in autoimmune pathogenesis. In this review, we discuss recent advances in understanding the mechanism of activation of AhR and its mediated functional regulation in various innate immune and lymphoid cell populations, as well as the immune-regulatory effect of AhR in the development of autoimmune diseases. In addition, we highlight the identification of AhR agonists and antagonists that may serve as potential therapeutic targets for the treatment of autoimmune disorders.

Application of propidium monoazide quantitative PCR to discriminate of infectious African swine fever viruses.

Introduction: The detection of African swine fever virus (ASFV) is commonly performed using quantitative real-time PCR (qPCR), a widely used virological method known for its high sensitivity and specificity. However, qPCR has a limitation in distinguishing between infectious and inactivated virus, which can lead to an overestimation of viral targets. Methods: To provide insights into ASFV infectivity, we evaluated the suitability of PMAxx, an improved version of propidium monoazide (PMA), as a means to differentiate between infectious and non-infectious ASFV. Pre-treatment with 50 µM PMAxx for 15 min significantly reduced the qPCR signal of ASFV in the live vaccine. Additionally, thermal treatment at 85°C for 5 min effectively inactivated the live ASFV in the vaccine. Based on a standard curve, the sensitivity of the PMAxx-qPCR assay was estimated to be approximately 10 copies/µL. Furthermore, we observed a strong agreement between the results obtained from PMAxx-qPCR and pig challenge experiments. Moreover, we utilized the PMAxx-qPCR assay to investigate the persistence of ASFV, revealing a close relationship between viral persistence and factors such as temperature and type of piggery materials. Conclusion: The findings of this study suggest that pre-treating viruses with PMAxx prior to qPCR is a reliable method for distinguishing between infectious and non-infectious ASFV. Thus, integrating of PMAxx-qPCR into routine diagnostic protocols holds potential for improving the interpretation of positive ASFV results obtained through qPCR.

Sublytic C5b-9 Induces CCL3/4 Production and Macrophage Accumulation in Thy-1N Rats via PKC-α/p65/IRF-8 Axis.

Mesangioproliferative glomerulonephritis (MsPGN) is a common human kidney disease. Rat Thy-1 nephritis (Thy-1N) is an animal model widely used for the study of MsPGN. Thy-1N is not only sublytic C5b-9-dependent, but also related to pro-inflammatory cytokine production and macrophage (Mφ) accumulation in rat renal tissues. In this study, we found that the expression or phosphorylation of chemokine CCL3/4, CD68 (Mφ marker), IRF-8, PKC-α and NF-κB-p65 (p65) were all up-regulated both in the renal tissues of Thy-1N rats (in vivo) and in the glomerular mesangial cells (GMCs) upon sublytic C5b-9 stimulation (in vitro). Further experiments in vitro revealed that the phosphorylated PKC-α (p-PKC-α) could promote p65 phosphorylation, and then p-p65 enhanced IRF-8 expression through binding to IRF-8 promotor (-591 ~ -582 nt and -299 ~ -290 nt). Additionally, up-regulation or silencing of IRF-8 gene promoted or reduced CCL3/4 production, and then regulated Mφ chemotaxis. The underlying mechanism involved in IRF-8 binding to CCL3 promoter (-249 ~ -236 nt), which resulted in CCL3 gene transcription. The experiments in vivo showed that knockdown of renal PKC-α, p65, IRF-8 and CCL3/4 genes could inhibit CCL3/4 production, Mφ accumulation, GMC proliferation and proteinuria of Thy-1N rats. Furthermore, p-PKC-α, p-p65, IRF-8, CCL3/4 expression and Mφ accumulation were also increased in the renal tissues of MsPGN patients. Collectively, these findings indicate that sublytic C5b-9 induces CCL3/4 production and Mφ accumulation via PKC-α/p65/IRF-8 axis, and finally aggravates the pathological changes of MsPGN.

Roles of IL-25 in Type 2 Inflammation and Autoimmune Pathogenesis.

Interleukin-17E (IL-25) is a member of the IL-17 cytokine family that includes IL-17A to IL-17F. IL-17 family cytokines play a key role in host defense responses and inflammatory diseases. Compared with other IL-17 cytokine family members, IL-25 has relatively low sequence similarity to IL-17A and exhibits a distinct function from other IL-17 cytokines. IL-25 binds to its receptor composed of IL-17 receptor A (IL-17RA) and IL-17 receptor B (IL-17RB) for signal transduction. IL-25 has been implicated as a type 2 cytokine and can induce the production of IL-4, IL-5 and IL-13, which in turn inhibits the differentiation of T helper (Th) 17. In addition to its anti-inflammatory properties, IL-25 also exhibits a pro-inflammatory effect in the pathogenesis of Th17-dominated diseases. Here, we review recent advances in the roles of IL-25 in the pathogenesis of inflammation and autoimmune diseases.

Adiponectin Enhances B-Cell Proliferation and Differentiation via Activation of Akt1/STAT3 and Exacerbates Collagen-Induced Arthritis.

Although B cells have been shown to contribute to the pathogenesis of rheumatoid arthritis (RA), the precise role of B cells in RA needs to be explored further. Our previous studies have revealed that adiponectin (AD) is expressed at high levels in inflamed synovial joint tissues, and its expression is closely correlated with progressive bone erosion in patients with RA. In this study, we investigated the possible role of AD in B cell proliferation and differentiation. We found that AD stimulation could induce B cell proliferation and differentiation in cell culture. Notably, local intraarticular injection of AD promoted B cell expansion in joint tissues and exacerbated arthritis in mice with collagen-induced arthritis (CIA). Mechanistically, AD induced the activation of PI3K/Akt1 and STAT3 and promoted the proliferation and differentiation of B cells. Moreover, STAT3 bound to the promoter of the Blimp-1 gene, upregulated Blimp-1 expression at the transcriptional level, and promoted B cell differentiation. Collectively, we observed that AD exacerbated CIA by enhancing B cell proliferation and differentiation mediated by the PI3K/Akt1/STAT3 axis.

IL-17 sustains the plasma cell response via p38-mediated Bcl-xL RNA stability in lupus pathogenesis.

Recent studies have demonstrated a central role for plasma cells in the development of autoimmune diseases, such as systemic lupus erythematosus (SLE). Currently, both the phenotypic features and functional regulation of autoreactive plasma cells during SLE pathogenesis remain largely unclear. In this study, we first found that a major subset of IL-17 receptor-expressing plasma cells potently produced anti-dsDNA IgG upon IL-17A (IL-17) stimulation in SLE patients and lupus mice. Using a humanized lupus mouse model, we showed that the transfer of Th17 cell-depleted PBMCs from lupus patients resulted in a significantly reduced plasma cell response and attenuated renal damage in recipient mice compared to the transfer of total SLE PBMCs. Moreover, long-term BrdU incorporation in lupus mice detected highly enriched long-lived BrdU+ subsets among IL-17 receptor-expressing plasma cells. Lupus mice deficient in IL-17 or IL-17 receptor C (IL-17RC) exhibited a diminished plasma cell response and reduced autoantibody production with attenuated renal damage, while the adoptive transfer of Th17 cells triggered the plasma cell response and renal damage in IL-17-deficient lupus mice. In reconstituted chimeric mice, IL-17RC deficiency resulted in severely impaired plasma cell generation but showed no obvious effect on germinal center B cells. Further mechanistic studies revealed that IL-17 significantly promoted plasma cell survival via p38-mediated Bcl-xL transcript stabilization. Together, our findings identified a novel function of IL-17 in enhancing plasma cell survival for autoantibody production in lupus pathogenesis, which may provide new therapeutic strategies for the treatment of SLE.

Effects of prostaglandin E combined with continuous renal replacement therapy on septic acute kidney injury.

BACKGROUND: The effects of prostaglandin E (PGE) combined with continuous renal replacement therapy (CRRT) on renal function and inflammatory responses in patients with septic acute kidney injury (SAKI) remain unclear. AIM: To investigate the effects of PGE combined with CRRT on urinary augmenter of liver regeneration (ALR), urinary Na+/H+ exchanger 3 (NHE3), and serum inflammatory cytokines in patients with SAKI. METHODS: The clinical data of 114 patients with SAKI admitted to Yichang Second People's Hospital from May 2017 to January 2019 were collected. Fifty-three cases treated by CRRT alone were included in a control group, while the other 61 cases treated with PGE combined with CRRT were included in an experimental group. Their urinary ALR, urinary NHE3, serum inflammatory cytokines, renal function indices, and immune function indices were detected. Changes in disease recovery and the incidence of adverse reactions were observed. The 28-d survival curve was plotted. RESULTS: Before treatment, urinary ALR, urinary NHE3, blood urea nitrogen (BUN), serum creatinine (SCr), CD3+ T lymphocytes, CD4+ T lymphocytes, and CD4+/CD8+ T lymphocyte ratio in the control and experimental groups were approximately the same. After treatment, urinary ALR and NHE3 decreased, while BUN, SCr, CD3+ T lymphocytes, CD4+ T lymphocytes, and CD4+/CD8+ T lymphocyte ratio increased in all subjects. Urinary ALR, urinary NHE3, BUN, and SCr in the experimental group were significantly lower than those in the control group, while CD3+ T lymphocytes, CD4+ T lymphocytes, and CD4+/CD8+ T lymphocyte ratio were significantly higher than those in the control group (P < 0.05). After treatment, the levels of tumor necrosis factor-α, interleukin-18, and high sensitivity C-reactive protein in the experimental group were significantly lower than those in the control group (P < 0.05). The time for urine volume recovery and intensive care unit treatment in the experimental group was significantly shorter than that in the control group (P < 0.05), although there was no statistically significant difference in hospital stays between the two groups. The total incidence of adverse reactions did not differ statistically between the two groups. The 28-d survival rate in the experimental group (80.33%) was significantly higher than that in the control group (66.04%). CONCLUSION: PGE combined with CRRT is clinically effective for treating SAKI, and the combination therapy can significantly improve renal function and reduce inflammatory responses.

The Roles of Immune Cells in the Pathogenesis of Fibrosis.

Tissue injury and inflammatory response trigger the development of fibrosis in various diseases. It has been recognized that both innate and adaptive immune cells are important players with multifaceted functions in fibrogenesis. The activated immune cells produce various cytokines, modulate the differentiation and functions of myofibroblasts via diverse molecular mechanisms, and regulate fibrotic development. The immune cells exhibit differential functions during different stages of fibrotic diseases. In this review, we summarized recent advances in understanding the roles of immune cells in regulating fibrotic development and immune-based therapies in different disorders and discuss the underlying molecular mechanisms with a focus on mTOR and JAK-STAT signaling pathways.

Aliskiren Improved the Endothelial Repair Capacity of Endothelial Progenitor Cells from Patients with Hypertension via the Tie2/PI3k/Akt/eNOS Signalling Pathway.

BACKGROUND: Studies show that aliskiren exerts favourable effects not only on endothelial progenitor cells (EPCs) but also on endothelial function. However, the mechanism of the favourable effect of aliskiren on EPCs from patients with hypertension is unclear and remains to be further studied. METHODS: The object of this study was to investigate and assess the in vitro function of EPCs pretreated with aliskiren. After treated with aliskiren, the human EPCs were transplanted into a nude mouse model of carotid artery injury, and the in vivo reendothelialization of injured artery was estimated by staining denuded areas with Evans blue dye via tail vein injection. RESULTS: We found that aliskiren increased the in vitro migration, proliferation, and adhesion of EPCs from patients with hypertension in a dose-dependent manner and improved the reendothelialization capability of these EPCs. Furthermore, aliskiren increased the phosphorylation of Tie2, Akt, and eNOS. After the blockade of the Tie2 signalling pathway, the favourable effects of aliskiren on the in vitro function and in vivo reendothelialization capability of EPCs were suppressed. CONCLUSIONS: This study demonstrates that aliskiren can improve the in vitro function and in vivo reendothelialization capability of EPCs from patients with hypertension via the activation of the Tie2/PI3k/Akt/eNOS signalling pathway. These findings further indicate that aliskiren is an effective pharmacological treatment for cell-based repair in hypertension-related vascular injury.

Overexpression of long noncoding RNA ANRIL inhibits phenotypic switching of vascular smooth muscle cells to prevent atherosclerotic plaque development in vivo.

BACKGROUND: Phenotypic switching of vascular smooth muscle cells (VSMCs) plays a key role in atherosclerosis. Long noncoding RNA ANRIL (lncRNA-ANRIL) is critical in vascular homeostasis. Metformin produces multiple beneficial effects in atherosclerosis. However, the underlying mechanisms need to be elucidated. METHODS AND RESULTS: Metformin increased lncRNA-ANRIL expression and AMPK activity in cultured VSMCs, and inhibited the phenotypic switching of VSMCs to the synthetic phenotype induced by platelet-derived growth factor (PDGF). Overexpression of lncRNA-ANRIL inhibited phenotypic switching and reversed the reduction of AMPK activity in PDGF-treated VSMCs. While, gene knockdown of lncRNA-ANRIL by adenovirus or silence of AMPKγ through siRNA abolished AMPK activation induced by metformin in VSMCs. RNA-immunoprecipitation analysis indicated that the affinity of lncRNA-ANRIL to AMPKγ subunit was increased by metformin. In vivo, administration of metformin increased the levels of lncRNA-ANRIL, suppressed VSMC phenotypic switching, and prevented the development of atherosclerotic plaque in Apoe-/- mice fed with western diet. These protective effects of metformin were abolished by infecting Apoe-/- mice with adenovirus expressing lncRNA-ANRIL shRNA. The levels of AMPK phosphorylation, AMPK activity, and lncRNA-ANRIL expression were decreased in human atherosclerotic lesions. CONCLUSION: Metformin activates AMPK to suppress the formation of atherosclerotic plaque through upregulation of lncRNA-ANRIL.

Endothelial progenitor cell impairment mediated vasodilation dysfunction via diminishing nitric oxide production in postmenopausal females.

Vascular endothelial dysfunction is the major contributing factor to hypertension. Endothelial progenitor cells (EPCs) are essential for endogenous vascular endothelial renovation. The activity and number of circulating EPCs are preserved in prehypertensive premenopausal females according to our previous research. However, the changes of EPCs in prehypertensive postmenopausal females are poorly understood, and the mechanisms responsible for the loss of the gender protection advantage of cardiovascular disease remain unexplored. In order to determine the effects of EPCs in prehypertensive postmenopausal females, the number and activity of circulating EPCs were tested in the present study. Next, the function of EPCs secreting nitric oxide (NO), vascular endothelial growth factor (VEGF) and granulocyte­macrophage colony­stimulating factor (GM­CSF), as well as their concentration in the plasma, were measured. The association between flow­mediated dilation (FMD) and EPC secretion was also assessed. Attenuation of proliferation and migration of EPCs was observed in prehypertensive patients in comparison with normotensive subjects. In addition, a reduced NO production secreted by EPCs was detected in prehypertensive patients as compared with that in normotensive patients. There was no significant difference in EPC function between postmenopausal females and age­matched males. Finally, the association between FMD and NO production was validated. Collectively, these data indicated that impaired EPCs mediated vasodilation dysfunction via decreasing NO production. Therefore, EPC function enhancement and NO level augmentation are emerging as novel therapeutic strategies for prehypertension therapy.

Attenuated endothelial function is associated with decreased endothelial progenitor cells and nitric oxide in premenopausal diabetic women.

Previous studies have demonstrated that the deleterious effect of diabetes mellitus (DM) on the risk of cardiovascular disease also occurs in premenopausal women, in spite of their relatively high estrogen levels; however, the underlying mechanism remains unclear. The present study aimed to investigate the sex­related differences in circulating endothelial progenitor cells (EPCs) in a relatively young population with type 2 DM (T2DM) and its underlying mechanism. The number and functional activity of circulating EPCs, and vascular endothelial function assessed using flow­mediated dilation (FMD), were compared in premenopausal women and age­matched men with or without T2DM. Nitric oxide (NO) in the plasma or NO secreted by EPCs was also measured. The number and activity of circulating EPCs, and NO levels in the plasma or culture medium, were lower in premenopausal women with T2DM compared with those without T2DM. In addition, the number and activity of circulating EPCs and NO levels were decreased in men with T2DM compared with in age­matched premenopausal women with T2DM. FMD was positively correlated with the number and activity of circulating EPCs, and NO levels. In conclusion, DM in premenopausal women may significantly impair the repair capability of EPCs and lead to endothelial dysfunction, which may be associated with reduced NO production. In patients with both DM and normal glucose tolerance, sex­related differences of EPCs are presented in a young population.

Downregulated GTCPH I/BH4 Pathway and Decreased Function of Circulating Endothelial Progenitor Cells and Their Relationship with Endothelial Dysfunction in Overweight Postmenopausal Women.

Endothelial progenitor cells (EPCs) have endogenous endothelium-reparative potential, but obesity impairs EPCs. Overweight premenopausal women have a normal number of circulating EPCs with functional activity, but whether EPCs in overweight postmenopausal women can repair obesity-related endothelial damage requires further investigation. For this purpose, we examined the function and number of circulating EPCs, evaluated vascular endothelial function, and explored the underlying mechanism. Compared with normal weight or overweight age-matched men, postmenopausal women (overweight or normal weight) had a diminished number of circulating EPCs and impaired vascular endothelial function, as detected by flow-mediated dilatation. Moreover, GTCPH I expression and the nitric oxide level in overweight postmenopausal women and men were significantly decreased. Together, our findings demonstrate that the number or function of circulating EPCs and endothelial function, which is partially regulated by the GTCPH I/BH4 signaling pathway, is not preserved in overweight postmenopausal women. The GTCPH I/BH4 pathway in circulating EPCs may be a potential therapeutic target for endothelial injury in overweight postmenopausal women.

Cardiac magnetic resonance and galectin-3 level as predictors of prognostic outcomes for non-ischemic cardiomyopathy patients.

This study was aimed at determining whether late gadolinium enhancement (LGE) in conjunction with Galectin-3 (Gal-3) level offered more precise prognosis of non-ischemic cardiomyopathy (NICM) in comparison to LGE alone. Results of LGE and Gal-3 expression in 192 patients with NICM, including 85 subjects with dilated cardiomyopathy (DCM) and 107 with hypertrophic cardiomyopathy (HCM), were examined. As suggested by the characteristics of LGE and Gal-3 levels, patients were divided into four groups: LGE positive + low Gal-3 (n = 10 for DCM, n = 15 for HCM), LGE positive + high Gal-3 (n = 25 for DCM, n = 51 for HCM), LGE negative + low Gal-3 (n = 32 for DCM, n = 29 for HCM), LGE negative + high Gal-3 (n = 18 for DCM, n = 12 for HCM). Primary endpoints over the follow-up period included major adverse cardiac events (MACEs). Kaplan-Meier survival analysis and univariate Cox proportional hazard models were used to analyze the survival status of patients with NICM. The optimal cut-off value of Gal-3 level for two types of NICM was determined by receiver operating characteristic analysis (13.38 U/L for DCM and 14.40 U/L for HCM). The combination of LGE and Gal-3 levels offered a more significant prognostic value than using LGE alone for both DCM and HCM (DCM P = 0.001 < 0.012; HCM P = 0.037 < 0.040). Moreover, the Cox proportional hazard model suggested that both LGE status [Hazard ratio (HR) = 2.62, P = 0.017] and Gal-3 level (HR = 1.16, P = 0.013) were significant predictors of MACEs in DCM, while they did not appear to have significant prognostic values for HCM (P = 0.06 and 0.64). Furthermore, the multivariate analysis only confirmed LGE as an independent element in predicting prognosis of DCM (HR = 12.19, P = 0.026). In conclusion, LGE status was an independent indicator of DCM prognosis, yet the insignificant role of LGE in HCM prognosis could be limited by sample size.

[Simultaneous transcatheter therapy for ventricular septal defect combined with atrial septal defect].

OBJECTIVE: To access the possibility, methods and efficacy of simultaneous transcatheter therapy for ventricular septal defect ( VSD ) combined with atrial septal defect (ASD). METHODS: In 68 patients with VSD, four patients ranging from 3 to 24 years old were combined with ASD. The diameters of perimembranous VSD were 2 approximately 10.5 mm, and the diameters of secundum ASD were 4.6 approximately 7 mm under the echocardiography before the operation. Another 4 patients with VSD occluded by left ventriculography: 3 patients were occluded by VSD occluder first, and then occluded by ASD occuder. The other was only occluded by VSD occluder. RESULTS: All VSD was treated successfully at one time in 4 patients. The diameters of VSD occluder were 4, 8, 10, and 16 mm. ASD was occluded successfully at one time in 3 patients. The diameters of ASD occluder were 8, 10, and 10 mm. The successful rate of the operation was 100%. No complication occurred in the operation and follow-up. CONCLUSION: Simultaneous transcatheter closure for VSD combined with ASD is a safe, feasible and effective therapy.

[Therapeutic effect and safety of transcatheter occlusion of ventricular septal defects in 50 patients].

OBJECTIVE: To determine the therapeutic effect and safety of transcatheter closure of ventricular septal defects (VSD) in 50 patients. METHODS: Fifty patients were diagnosed by transthoracic echocardiography. To perform the operation, transthoracic echocardiography and X ray were used continuously to monitor the procedure. Transthoracic echocardiography and ECG were performed at 1, 3, and 6 months after the operation to evaluate the therapeutic effect. RESULTS: The VSD diameter ranged from 1.8 to 13.4 (5.54 +/- 2. 75) mm. The successful rate of the operation was 96.0%, and the complication rate of the operation was 16.7%. A 3 month follow-up was completed in 20 patients, and the median left ventricle end-diastolic dimension significantly decreased from (40.20 +/- 8.80) mm to (32.90 +/- 8.36) mm (P < 0.001). CONCLUSION: Transcatheter closure of ventricular septal defects is a good method with a high success rate of placement, fewer complications, and a good occlusion effect.

[Formation and function of coronary collateral circulation and their influencing factors].

OBJECTIVE: To clarify the formation and function of coronary collateral circulation (CCC) in coronary artery disease (CAD) patients with severe coronary artery stenosis and their influencing factors. METHODS: Coronary angiography was performed on 266 CAD patients with severe coronary stenosis. CCC formation was evaluated by Rentrop rating on those 266 patients and 401 severe stenosis arteries; while in CCC formed patients, CCC function was evaluated by Werner collateral collection (CC) rating. The formation, function of CCC and their influencing factors were analyzed and compared. RESULTS: CCC formation in those severe stenosis coronary arteries was related to the severity of coronary stenosis: the forming rate of CCC was 42.6% in vessels with 90%-94% stenosis (Group A), 56.9% with 95%-99% stenosis (Group B) and 93.0% with 100% stenosis (Group C) (p <0 .01). Between CCC forming and non-forming groups, there was no significant difference in age, gender, incidence of MI, hypertension and diabetes, history of smoking and serum levels of HDL-C and LDL-C (P > 0.05). In the CCC formation group, serum HDL-C level was the highest in the CC Grade 2 group (according to Werner function rating) and the lowest in the CC Grade 0 group (P < 0.05). Whereas, LDL-C level was the lowest in the CC Grade 2 group and the highest in the CC Grade 0 group (P < 0.05). CONCLUSION: Severity of coronary stenosis was the major influencing factor in CCC formation and function, and the rate of CCC formation increased with the exacerbation of coronary stenosis. Serum HDL-C and LDL-C level had no relationship with CCC formation, but related to CCC function. Better CCC function was found in patients with high level of HDL-C whereas the patients with high level of LDL-C had spoiled CCC function.