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Kidney is a highly vascularized organ and peritubular capillary network constitutes the critical component of its microvascular system. Peritubular capillaries, as the main vessels for blood supply in renal tubules and renal interstitium, involve in important physiological processes in renal tubules such as energy metabolism, substance secretion and reabsorption. In recent years, it has been demonstrated that ischemia-reperfusion injury, rejection and renal fibrosis during kidney transplantation would result in compromised structural integrity and decreased number in peritubular capillaries, thus leading to interstitial fibrosis in renal allograft, which would seriously affect the long-term stability of renal function in the renal allograft. Therefore, we reviewed the structure and function of peritubular capillary, peritubular capillary and ischemia-reperfusion injury, rejection and renal allograft fibrosis, focusing on the mechanism for peritubular capillary injury in kidney transplantation and the specific changes manifested, with the aim of providing a reference for preventing and treating perioperative complications in kidney transplantation and improving the long-term prognosis of grafts.
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@#AIM: To explore the changes of retinal optical coherence tomography angiography(OCTA)vessel density in Patients with Alzheimer's disease(AD)by Meta-analysis, and to explore the value of OCTA in early diagnosis of AD patients.<p>METHODS: Embase, PubMed and Cochrane Library data were searched from January 2016 to September 2021 for relevant studies on vessel density in macular area of AD patients. Two researchers independently screened the literature, extracted the data, and evaluated the risk of inclusion bias using Newcastle-Ottawa Scale(NOS). Meta-analysis was performed using RevMan 5.3 software.<p>RESULTS: A total of 740 cases(eyes)were included in 10 literatures, including 321 cases from the AD group and 419 cases from the control group(age-matched people with normal cognitive abilities). The results of the Meta-analysis showed that the superficial vessel density in macular area of AD patients was lower than that in control group(<i>MD</i>=-1.58, 95%<i>CI</i> -2.60- -0.55, <i>P</i>=0.003). The deep vessel density in macular area of AD patients was lower than that in control group(<i>MD</i>=-2.72, 95%<i>CI</i> -4.36- -1.07, <i>P</i>=0.001). The parafoveal vessel density in AD patients was lower than that in control group(<i>MD</i>=-1.44, 95%<i>CI</i> -1.94- -0.94, <i>P</i><0.00001). The avascular area in the fovea of AD patients was slightly larger than that of the control group(<i>MD</i>=0.05, 95%<i>CI</i> -0.01-0.11, <i>P</i>=0.13).<p>CONCLUSION: The vessel density of each layer in macular area of AD patients were lower than that of control groups the difference was statistically significant. OCTA can assist in the early diagnosis of AD.
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Systemic sclerosis (SSc) is a chronic autoimmune disease that can involve multiple organs throughout the body. It is characterized by extensive vascular disease and fibrosis of the skin and internal organs, but its mechanism is still unclear. Studies have confirmed that the Wnt pathway is involved in SSc fibrosis, but its pathological role in vascular lesions has not been reported. In this study, the bleomycin (BLM)-induced SSc mouse model was used to investigate the role of Wnt pathway in SSc cutaneous vascular lesions. Eighteen BALB/C mice were randomly divided into control, model and treatment groups. The control group of mice was injected with PBS 100 μL/d. The model group was injected with BLM 100 μL/d at a concentration of 1 mg/mL. The treatment group of mice received injection of BLM 100 μL as the model group of mice and retroperitoneal injection of iCRT3 (Wnt and beta-catenin inhibitors) 5 mg/kg/d. Mice were sacrificed on day 28. The thickness of dorsal dermis and epidermis in the model group induced by BLM was significantly higher than that in the control group (P <0. 05). The skin appendages such as sebaceous glands and hair follicles in the model group were significantly reduced. At the same time, the thickness of fat layer became thinner and surrounded by fibrous tissue, and the collagen deposition in the model group was higher than that in the control group. It was identified at the histological level by immunohistochemical staining that α-SMA expression in model group and treatment group α-SMA is highly expressed in skin tissues, and the positive expression of α-SMA around blood vessels was significantly higher than that in the control group. In addition, the expression of IL-6 and IL-17 in serum of model group was significantly higher than that in control group (P<0. 05), and the expression of IL-6 and IL-17 in serum of treatment group was significantly lower than that in model group (P<0. 05). Furthermore, q-PCR analysis showed that the mRNA levels of β-catenin in the skin microvessels of the mice were higher in the model and the treatment groups as compared with the control group. The protein levels of Wnt5A, β-catenin, α-SMA and col1A1 were analyzed by Western blotting and results showed that the levels of fibrosis-related proteins, α-SMA and col1A1, were increased in the model group injected with BLM as compared with the control group (P<0. 05), whereas iCRT3 treatment attenuated the upregulation of α-SMA and col1A1 induced by BLM in the treatment group (P<0. 05). The levels of Wnt pathway-related proteins β-catenin and Wnt5A were significantly increased in the model group as compared with the control (P<0. 05). This study suggests that BLM can successfully induce the skin phenotype of mice with systemic sclerosis. Abnormal activation of Wnt signaling pathway is involved in BLM-induced skin microangiopathy in mice with scleroderma, and the specific Wnt pathway inhibitor iCRT3 can reduce BLM-induced scleroderma. The expression of α-SMA and col1A1 proteins in mouse skin microvessels can improve the microvascular lesions of mouse skin. Inhibition of Wnt pathway may directly or indirectly down-regulate the abnormal expression of cytokines IL-6 and IL-17, and interfere with BLM-induced progression of vascular lesions in mice.
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Objective To investigate the mechanisms underlying the effect of 5-aminolevulinic acid photodynamic therapy (ALA-PDT) on cutaneous squamous cell carcinoma (SCC) in mice.Methods A model of cutaneous SCC was established in 21 SKH-1 hairless mice,which were treated with topical ALA 8％ cream followed by single irradiation with He-Ne laser at a total dose of 30 J/cm2 (ALA-PDT).Three mice were sacrificed before and at 1,3,6,12,24 hours and 7 days after the irradiation,separately,and SCC tissue was taken from the mice.Transmission electron microscopy (TEM) and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) were performed to determine the pattern of tumor cell death(necrosis,apoptosis and autophagy) during 1-24 hours after ALA-PDT,and immunohistochemical techniques were used to estimate the expressions of LC3B and CD34 on SCC cells,as well as the quantity of CD1a+ cells,CD4+ T and CD8+ T lymphocytes in SCC tissue 7 days after the irradiation.Statistical analysis was done by two-sample t test using SPSS 17.0 software.Results TEM showed gradual necrosis and apoptosis (especially necrosis) of tumor cells and formation of autophagosomes in macrophages within 24 hours after ALA-PDT.The number of apoptotic cells per high power field (× 400) in SCC tissue significantly increased at 24 hours compared with that before ALA-PDT (7.30 ± 2.18 vs.2.00 ± 0.69,P ＜ 0.05).As immunohistochemistry revealed,there was a significant decrease in the number of CD34+ cells (1.33 ± 0.58 vs.19.00 ± 2.66,P＜ 0.01),but a marked increase in that of CD1a+ ce1ls (23.01 ± 2.04 vs.10.33 ± 1.88,P＜ 0.05),CD4+ T cells (28.67 ± 1.76 vs.12.40 ± 2.27,P＜ 0.05),CD8+ T cells (25.79 ± 2.37 vs.11.67 ± 1.45,P ＜ 0.05) and LC3B+ interstitial cells (30.6 ± 3.21 vs.21.44 ± 4.3,P ＜ 0.05) per high power field (× 400) in SCC tissue on day 7 compared with that before ALA-PDT.Conclusions ALA-PDT may directly kill SCC cells by inducing cell necrosis and apoptosis rather than autophagy.Additionally,ALA-PDT can injure microvascular endothelial cells and cause the aggregation of dendritic cells,CD4+ T cells and CD8+ T cells in SCC tissue.