Effect of Beclin-1 gene silencing on autophagy and apoptosis of the prostatic hyperplasia epithelial cells.

OBJECTIVES: This study aims to explore the effect of silencing Beclin-1 gene on autophagy and apoptosis of Benign Prostatic Hyperplasia (BPH) (BPH-1) cells under the condition of Androgen Deprivation (AD) and Autophagy Inhibition (AI). METHODS: Control group (BPH-1 group), empty carrier group (sh-RNA-BPH-1 group) and Beclin-1 silenced group (sh-Beclin1-BPH-1 group) were set. The Beclin-1 gene silencing efficiency was detected by RT-PCR and Western blot. Autophagic flux was monitored by GFP-LC3 cleavage assay and cell apoptosis was analyzed by flow cytometry. The protein expression levels of LC3, Caspase-3, PARP-1, Bcl-2, and Bax were detected by Western blot. RESULTS: The transfection of sh-Beclin-1 obviously down-regulated the expression of Beclin-1 at both mRNA and protein levels. Under the conditions of AD and AI, silencing of Beclin-1 restrained the autophagy of BPH-1 cells, as evidenced by a decreased number of autophagosomes and down-regulation of LC3-II protein (p < 0.001). The results of flow cytometry showed that the apoptotic rate of sh-Beclin-1 group was elevated significantly compared to the other two groups (p < 0.01). Western blot results showed that silencing of Beclin-1 promoted 89 kd fragmentation of PARP-1 (p < 0.001) and Caspase-3 activation (p < 0.01). Moreover, silencing of Beclin-1 resulted in declined Bcl-2 and augmented Bax protein expression in BPH-1 cells (p < 0.01), which ultimately led to a decreased Bcl-2/Bax ratio. CONCLUSIONS: The results indicated that the silencing of Beclin-1 gene hampered autophagy while activating apoptosis in BPH-1 cells. Thus, Beclin-1 may participate in an antagonistic relationship between autophagy and apoptosis in BPH.

Effect of Beclin-1 gene silencing on autophagy and apoptosis of the prostatic hyperplasia epithelial cells

Abstract Objectives: This study aims to explore the effect of silencing Beclin-1 gene on autophagy and apoptosis of Benign Prostatic Hyperplasia (BPH) (BPH-1) cells under the condition of Androgen Deprivation (AD) and Autophagy Inhibition (AI). Methods: Control group (BPH-1 group), empty carrier group (sh-RNA-BPH-1 group) and Beclin-1 silenced group (sh-Beclin1-BPH-1 group) were set. The Beclin-1 gene silencing efficiency was detected by RT-PCR and Western blot. Autophagic flux was monitored by GFP-LC3 cleavage assay and cell apoptosis was analyzed by flow cytometry. The protein expression levels of LC3, Caspase-3, PARP-1, Bcl-2, and Bax were detected by Western blot. Results: The transfection of sh-Beclin-1 obviously down-regulated the expression of Beclin-1 at both mRNA and protein levels. Under the conditions of AD and AI, silencing of Beclin-1 restrained the autophagy of BPH-1 cells, as evidenced by a decreased number of autophagosomes and down-regulation of LC3-II protein (p < 0.001). The results of flow cytometry showed that the apoptotic rate of sh-Beclin-1 group was elevated significantly compared to the other two groups (p < 0.01). Western blot results showed that silencing of Beclin-1 promoted 89 kd fragmentation of PARP-1 (p < 0.001) and Caspase-3 activation (p < 0.01). Moreover, silencing of Beclin-1 resulted in declined Bcl-2 and augmented Bax protein expression in BPH-1 cells (p < 0.01), which ultimately led to a decreased Bcl-2/Bax ratio. Conclusions: The results indicated that the silencing of Beclin-1 gene hampered autophagy while activating apoptosis in BPH-1 cells. Thus, Beclin-1 may participate in an antagonistic relationship between autophagy and apoptosis in BPH.

Risk factors for ureteroscopic lithotripsy: a case-control study and analysis of 385 cases of holmium laser ureterolithotripsy.

INTRODUCTION: Ureteroscopic lithotripsy has become the first choice for the treatment of middle and lower ureteral stones, but it still has a certain rate of surgical failure. Here we aimed to determine the factors that may affect the success rate of holmium laser ureterolithotripsy (HLU) and provide the basis and guidance for its future use. AIM: To evaluate the risk factors for HLU failure. MATERIAL AND METHODS: The clinical data of 385 patients undergoing holmium laser ureterolithotripsy from 2009 to 2012 were retrospectively reviewed to analyze the impact of gender, age, stone side, stone size, stone location, stone number, degree of hydronephrosis, stone impaction, previous extracorporeal shock lithotripsy (ESWL), and associated urinary tract infection (UTI) on the success or failure of surgery. RESULTS: Surgical success was achieved in 338 (87.8%) patients versus surgical failure in 47 (12.2%) patients. Univariate analysis revealed that the degree of hydronephrosis (p = 0.024), stone impaction (p = 0.003), stone location (p = 0.012), and previous ESWL (p = 0.037) were risk factors for surgical failure. Multivariate logistic regression revealed that stone impaction (odds ratio (OR) = 2.66; p = 0.018) and stone location (OR = 2.11; p = 0.013) were significantly associated with surgical failure. Since some cases of ureterostenosis developed postoperatively, we continued follow-up. The patients had the stent for a year and underwent regular follow-up checks until 5 years. No cases of ureterostenosis recurred. CONCLUSIONS: Ureteroscopic lithotripsy is a safe procedure with few complications. Stone impaction and proximal location are the risk factors for its failure.

Long noncoding RNA (MEG3) in urinal exosomes functions as a biomarker for the diagnosis of Hunner-type interstitial cystitis (HIC).

BACKGROUND: Toll-like receptor-7 (TLR7) is functionally involved in the pathogenesis of Hunner-type interstitial cystitis (HIC). In addition, maternally expressed gene 3 (MEG3) is implicated in many urethral diseases. In this study, we aimed to verify the hypothesis that exosomal MEG3 in urine can be used as a novel diagnostic biomarker for HIC. METHODS: Electron microscopy was utilized to observe the distribution of urinary exosomes between the case group and the control group. Receiver operating characteristic analysis was utilized to compare the diagnostic values of MEG3 and miR-19a-3p. Computational analysis and luciferase assay were conducted to identify the correlation between MEG3 and miR-19a-3p as well as between TLR7 and miR-19a-3p. In addition, real-time polymerase chain reaction and Western blot were performed to establish the signaling pathways implicated in the pathogenesis of HIC. RESULTS: When age and gender distributions are excluded, urinary exosomes were equally distributed between case and control groups. The area under the curve of MEG3 was larger than that of miR-19a-3p, indicating that MEG3 has a better value in the diagnosis of HIC. In addition, patients with HIC showed elevated MEG3 expression and inhibited miR-19a-3p expression, thus establishing a negative correlation between MEG3 and miR-19a-3p. MEG3 and TLR7 were both identified as targets of miR-19a-3p, establishing a MEG3/miR-19a-3p/TLR7 signaling pathway, in which MEG3 enhances the expression of TLR7 via inhibiting the expression of miR-19a-3p. CONCLUSION: MEG3 level was upregulated in patients with HIC. In addition, MEG3 downregulated miR-19a-3p expression while upregulating TLR7 expression. Furthermore, MEG3 contributes to the pathogenesis of HIC. Therefore, exosomal MEG3 in urine can be used as a biomarker for HIC diagnosis.

LINC01638 lncRNA promotes the proliferation, migration and invasion of prostate carcinoma cells by interacting with Notch1.

LINC01638 lncRNA is known as an oncogenic lncRNA in triple negative breast cancer. However, the role of LINC01638 lncRNA in other diseases is unknown. In the present study we observed that plasma levels of LINC01638 lncRNA and Notch1 were upregulated in prostate carcinoma patients comparing with healthy controls. LINC01638 lncRNA and Notch1 were positively correlated in prostate carcinoma patients but not in healthy controls. Upregulation of LINC01638 lncRNA distinguished prostate carcinoma patients from healthy controls. LINC01638 lncRNA overexpression in prostate carcinoma cells led to upregulated Notch1 expression. Notch1 overexpression also led to increased expression level of LINC01638 lncRNA. Both LINC01638 lncRNA and Notch1 overexpression promoted the proliferation, migration and invasion of prostate carcinoma cells. We concluded that LINC01638 lncRNA might promote the proliferation, migration and invasion of prostate carcinoma cells by interacting with Notch1.

Serum exosomal miR-210 as a potential biomarker for clear cell renal cell carcinoma.

Exosomal microRNAs (miRNAs) are suggested to reflect molecular changes occurring in their cells of origin and are potential indicators in the early detection of cancers. This study aimed to determine whether certain exosomal miRNAs from tumor tissue can be used as noninvasive biomarkers for clear cell renal cell carcinoma (ccRCC). Based on ccRCC miRNA expression profiles and the literature, we selected six miRNAs (miR-210, miR-224, miR-452, miR-155, miR-21, and miR-34a) and analyzed their expression in tissues, sera, and serum exosomes through quantitative real-time polymerase chain reaction in hypoxia-induced (with CoCl2 ) renal cell lines. miR-210, miR-224, miR-452, miR-155, and miR-21 were upregulated in tumor tissues compared with normal tissues. Serum miR-210 and miR-155 levels were higher in patients with ccRCC than in healthy controls (HCs). Furthermore, only exosomal miR-210 was significantly upregulated in patients with ccRCC than in HCs. Moreover, receiver operating characteristic (ROC) curve analysis revealed an area under the ROC curve of 0.8779 (95% confidence interval, 0.7987-0.9571) and a sensitivity and specificity of 82.5% and 80.0%, respectively. Moreover, exosomal miR-210 was upregulated at an advanced stage, and Fuhrman grade and metastasis decreased significantly one month after surgery. Acute hypoxia exposure activates miR-210 and release of exosomes with upregulated miR-210 in both normal and tumor RCC cell lines and interferes with vacuole membrane protein 1 mRNA expression, especially in the metastatic ccRCC cell line. In conclusion, Serum exosomal miR-210 originating from tumor tissue has potential as a novel noninvasive biomarker for the detection and prognosis of ccRCC.

Detection of urinary trace elements and pattern recognition analysis in patients with renal cell carcinoma by inductively coupled plasma mass spectrometry.

OBJECTIVE: This study aims to observe the changes and diagnostic values of urinary trace elements in patients with renal cell carcinoma (RCC). METHODS: A total of 28 RCC patients that had been performed radical surgery for more than 3 years were included into this case-control study; meanwhile, thirty healthy volunteers without kidney diseases were set as the control group over the same period. The levels of various urinary trace elements in both groups were measured, and the results were performed the significance analysis and pattern recognition analysis using with partial least square discriminant analysis and Fisher analysis. RESULTS: The significance analysis showed that compared with the control group, the case group exhibited significantly reduced levels of Mg (26.3 mg/L for the case group vs. 52.1 mg/L for the control group, P < 0.05), V (72.9 µg/L for the case group vs. 110.1 µg/L for the control group, P < 0.05), Mo (59.6 µg/L for the case group vs. 261.7 µg/L for the control group, P < 0.05), and Sn (4.5 µg/L for the case group vs. 27.3 µg/L for the control group, P < 0.05) while significantly increased Cd (25.0 µg/L for the case group vs. 15.5 µg/L for the control group, P < 0.05). The accuracy of the discriminant function established by the Fisher analysis was 91.4%. CONCLUSIONS: Patients with RCC exhibit differences in such urinary trace elements as Mg, V, Mo, Sn, and Cd with healthy populations, and the discriminant accuracy is high.

Circular RNA CEP128 acts as a sponge of miR-145-5p in promoting the bladder cancer progression via regulating SOX11.

BACKGROUND: This study aimed to investigate the effect of over-expressing circular RNA CEP128 (circCEP128) on cell functions and explore the molecular mechanism of which in bladder carcinoma. METHODS: The differentially expressed circRNAs and mRNAs in bladder carcinoma cells and cells in adjacent tissues were screened out using microarray analysis. Expression levels of circRNAs and mRNAs in tissues and cells were determined by qRT-PCR. Expression of SOX11 was detected by western blot. Luciferase reporter assay and RNA pull-down assay were used to investigate the interactions between the specific circRNA, miRNA and mRNA. Cell cycle and apoptosis were measured using flow cytometry after transfection. MTT assay was also performed to detect the cell proliferation. RESULTS: In present study, circCEP128 and SOX11 were observed significantly up-regulated in bladder cancer tissues, while the expression of miR-145-5p was decreased in cancer samples compared to normal samples. Cytoscape was used to visualize circCEP128-miRNA-target gene interactions based on the TargetScan and circular RNA interactome, which revealed that circCEP128 served as a sponge of miR-145-5p and indirectly regulated SOX11. Knockdown of circCEP128 induced the inhibition of cell proliferation and the increased bladder cancer cell apoptosis rate. CONCLUSIONS: CircCEP128 functions as a ceRNA for miR-145-5p, which could up regulates SOX11 and further promotes cell proliferation and inhibits cell apoptosis of bladder cancer.

Crosstalk between apoptosis and autophagy in prostate epithelial cells under androgen deprivation.

The present study investigated the molecular mechanism of apoptosis and autophagy in prostate epithelial cells under androgen deprivation (AD). BPH-1 cells were divided into four groups as follows: Control (Cont), AD, autophagy inhibition (AI) and AD + AI groups. Cells in the four groups were treated accordingly, and the level of apoptosis was subsequently measured via flow cytometry. The expression of the microtubule-associated proteins 1A/1B light chain 3 (LC3), caspase-3, poly (ADP-ribose) polymerase 1 (PARP-1) and Beclin-1 proteins of BPH-1 cells was detected at different time points following culture in androgen-deprived medium. Western blotting revealed that the basal levels of the LC3-II protein were detected at 0 h. At 4 h, LC3-II was significantly increased compared with 0 h (P<0.05). Beginning at 20 h, the expression level of the LC3-II protein decreased significantly (P<0.05). Western blotting revealed that beginning at 24 h, the expression level of the PARP-1 protein decreased significantly (P<0.001) and the cleavage fragments of the PARP-1 protein appeared. These results further imply that autophagy serves a cell protective function by mutual inhibition with apoptosis in BPH-1 cells in the removal of androgen conditions. Furthermore, the fragments of the cleaved Beclin-1 protein appeared as 35 and 37 kDa bands. Flow cytometry analysis demonstrated that the rate of cell apoptosis in the AD, AI and AD + AI groups was significantly increased compared with the Cont group (P<0.01). Compared with the AD or the AI groups individually, the rate of cell apoptosis in the AD + AI group was significantly increased (P<0.001). These findings suggest that in the early stage of AD, autophagy has a compensatory function in the cell, whereas in the whole process, autophagy and apoptosis share a mutual antagonism. The Beclin-1-C protein fragment contributed positive feedback to the process of apoptosis, which may be a potential mechanism of AD therapy. Therefore, AD and AI exhibit a synergistic effect to further improve the level of apoptosis.

Roles of autophagy in androgen-induced benign prostatic hyperplasia in castrated rats.

The present study investigated the role of androgen in the process of androgen-induced prostate hyperplasia in castrated rats and assessed the role of the phosphoinositide 3-kinase/protein kinase B/mechanistic target of rapamycin (PI3K/Akt/mTOR) pathway in this process. Furthermore, the extent to which autophagy may affect the level of androgen-induced benign prostatic hyperplasia was also explored. A total of 40 Sprague Dawley rats were randomly divided into four groups: Testosterone group, rapamycin group, 3-methyladenine (3-MA) group, and control group. The extent of hyperplasia in prostate tissue the apoptosis and autophagy were assayed. The prostate wet weight, volume and index in the testosterone group were significantly higher compared with the control group (P<0.05) and these factors were significantly lower in the rapamycin group compared with the testosterone group (P<0.05). HE staining demonstrated that prostate hyperplasia was obvious in the testosterone group. Western blotting revealed that caspase-3 levels were higher in the 3-MA group compared with the control group and Bcl-2 was higher in the testosterone group compared with the control group (P<0.05). Furthermore, in the rapamycin group, Bcl-2 protein expression levels were significantly lower than those in the testosterone group (P<0.05). The prostate tissue was analyzed using electron microscopy and autophagy bodies were identified in the rapamycin group. In the process of androgen-induced prostatic hyperplasia in castrated rats, the role of androgen may be related to the PI3K/Akt/mTOR signaling pathway. Rapamycin was able to inhibit the effect of testosterone and promoted prostate tissue hyperplasia by inhibiting the PI3K/Akt pathway. In addition to inhibiting apoptosis in prostate cells, androgen was able to induce rat prostate hyperplasia and may also be related to the promotion of the proliferation of prostate cells.

Association between CD40 rs1883832 and immune-related diseases susceptibility: A meta-analysis.

BACKGROUND/OBJECTIVE: It has been reported that CD40 rs1883832 might be associated with immune-related diseases susceptibility. Owing to mixed and inconclusive results, we conducted a meta-analysis of case-control studies to summarize and clarify this association. METHODS/MAIN RESULTS: A systematic search of studies on the association between CD40 rs1883832 and immune-related diseases susceptibility was conducted in databases. Odds ratios and 95% confidence intervals were used to pool the effect size. 40 articles were included in our meta-analysis. CONCLUSIONS: CD40 rs1883832 is associated with decreased risk of Graves' disease, especially in Asian; CD40 rs1883832 is associated with increased risk of multiple sclerosis; CD40 -1C>T (rs1883832) is not associated with the susceptibility of Hashimoto's thyroiditis, systemic sclerosis or Asthma; there is insufficient data to fully confirm the association between CD40 rs1883832 and systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), Behçet's disease (BD), myasthenia gravis (MG), Crohn's disease (CD), ulcerative colitis (UC), Sarcoidosis, Fuch uveitis syndrome (FUS), Vogt-Koyanagi-Harada syndrome (VKH), Kawasaki disease (KD), giant cell arteritis (GCA) or Immune thrombocytopenia (ITP).

[Target protein candidates of hypothalamus in aging rats with intervention by Qiongyugao].

To explore the associated proteins of the hypothalamus in aging rat models with intervention by Qiongyugao(QYG) based on iTRAQ technology, find out the target protein candidates and investigate the mechanism of delaying aging for Qiongyugao. The results showed that Qiongyugao increased GSH-Px activity in serum and SOD activity in liver; the total protein count identified by iTRAQ was 3 522, FDR<1%. There were 20 kinds of differential proteins between the blank group and model group; there were 295 kinds of differential proteins between model group and QYG group, and 40 kinds of them had a difference multiple ≥1.30 (the maximum value was 1.47). Compared with blank group, there were 14 kinds of proteins that were down-regulated in model group and up-regulated in QYG group. Combined with literature search and gene function search, 12 kinds of target protein candidates were screened out ： ST18, Ptprc, PSMB8, INPP4B, Shc3, Pik3r1, PIP5K1C, Nampt, Rasgrp2, Asah2, Pdpk1, and Map2k7. The expression of nuclear factor-kappa B (NF-κB) in the hypothalamic inflammatory pathway was detected by Western blot and the results showed that its expression level in model group(0.96) was higher than that in control group(0.85), while its expression level in QYG group(0.89) was lower than that in model group. Q-PCR results showed that the relative mRNA expression levels of PIP5K1C and Ptprc in model group were significantly lower than those in blank group(P<0.01); while compared with the model group, the mRNA expression levels of PIP5K1C and Ptprc in QYG group were significantly increased(P<0.01) . This result was consistent with proteomics data. QYG may delay aging by regulating hypothalamic inflammatory reaction.

Treatment of hematuria caused by renal arteriovenous malformation in pregnant patients.

This study is to investigate hematuria in pregnant patients caused by renal arteriovenous malformation and to evaluate the efficacy of superselective renal angiography and embolization used for treatment of renal arteriovenous malformation. Two cases of hematuria in pregnant patients caused by renal arteriovenous malformation were enrolled. Case 1 was a 28-year-old woman with repeatedly intermittent hematuria at week 7 during gestation. Case 2 was a 30-year-old woman with repeatedly intermittent hematuria at week 8 during gestation. B ultrasound and CT were performed to detect hydronephrosis. Renal arteriovenous malformation was diagnosed by selective angiography. Both the patients were treated with embolization. The 2 cases were successfully embolized with different materials including gelfoam and coils. Both of the 2 patients were recovered well and discharged successful after the operation. In conclusion, superselective renal angiography and embolization are effective methods for diagnosis and treatment of renal arteriovenous malformation in pregnant patients.

Pygopus 2 promotes kidney cancer OS-RC-2 cells proliferation and invasion in vitro and in vivo.

OBJECTIVE: Human Pygopus 2 (Pygo2) was recently discovered to be a component of the Wnt signaling pathway required for ß-catenin/Tcf-mediated transcription. But the role of Pygo2 in malignant cell proliferation and invasion has not yet been determined. METHODS: Lentivirus-mediated small interfering RNA (siRNA) and vector-based overexpression were used to study the function of Pygo2 in OS-RC-2 cells. The resulted cells were subject to Western blotting assay, MTT assay, colony formation and cell invasion assays. Furthermore, renal cell carcinoma (RCC) models were established in BALB/c nude mice inoculated with OS-RC-2 cells. Immunohistochemistry (IHC) staining of matrix metalloproteinase-7 (MMP-7), matrix metalloproteinase-9 (MMP-9) and vascular endothelial growth factor (VEGF) was performed in tumor tissue. RESULTS: Pygo2 gene was successful knocked down and overexpressed in RCC OS-RC-2 cells by using an shRNA and overexpressing vector, respectively. Overexpression of Pygo2 effectively promoted cell proliferation, colony formation and invasion in vitro. Knockdown of Pygo2 obviously inhibited xenograft tumor growth in nude mice. In addition, overexpression of Pygo2 increased the levels of MMP-7, MMP-9 and VEGF in the xenograft tumors. CONCLUSION: Pygo2 has a role in promoting cell proliferation, invasion and metastasis, and may regulate angiogenesis via the Wnt/ß-catenin signaling pathway.

Practical, modular, and general synthesis of 3-coumaranones through gold-catalyzed intermolecular alkyne oxidation strategy.

A gold-catalyzed intermolecular alkyne oxidation for the preparation of 3-coumaranones has been developed. Using 8-isopropylquinoline N-oxides as oxidants, the reactions of o-ethynylanisoles afford versatile 3-coumaranones in moderate to good isolated yields. The synthetic utility of this chemistry is also indicated by the synthesis of the natural product sulfuretin.

A double-negative feedback loop between Wnt-ß-catenin signaling and HNF4α regulates epithelial-mesenchymal transition in hepatocellular carcinoma.

Wnt-ß-catenin signaling participates in the epithelial-mesenchymal transition (EMT) in a variety of cancers; however, its involvement in hepatocellular carcinoma (HCC) and downstream molecular events is largely undefined. HNF4α is the most prominent and specific factor maintaining the differentiation of hepatic lineage cells and a potential EMT regulator in HCC cells. However, the molecular mechanisms by which HNF4α maintains the differentiated liver epithelium and inhibits EMT have not been completely defined. In this study, we systematically explored the relationship between Wnt-ß-catenin signaling and HNF4α in the EMT process of HCC cells. Our results indicated that HNF4α expression was negatively regulated during Wnt-ß-catenin signaling-induced EMT through Snail and Slug in HCC cells. In contrast, HNF4α was found to directly associate with TCF4 to compete with ß-catenin but facilitate transcription co-repressor activities, thus inhibiting expression of EMT-related Wnt-ß-catenin targets. Moreover, HNF4α may control the switch between the transcriptional and adhesion functions of ß-catenin. Overexpression of HNF4α was found to completely compromise the Wnt-ß-catenin-signaling-induced EMT phenotype. Finally, we determined the regulation pattern between Wnt-ß-catenin signaling and HNF4α in rat tumor models. Our studies have identified a double-negative feedback mechanism controlling Wnt-ß-catenin signaling and HNF4α expression in vitro and in vivo, which sheds new light on the regulation of EMT in HCC. The modulation of these molecular processes may be a method of inhibiting HCC invasion by blocking Wnt-ß-catenin signaling or restoring HNF4α expression to prevent EMT.

The use of chitosan based hydrogel for enhancing the therapeutic benefits of adipose-derived MSCs for acute kidney injury.

Transplantation of mesenchymal stem cells (MSCs) has been reported a great therapeutic potential for acute kidney injury (AKI). However, the therapeutic benefits are limited due to the low retention and survival of transplanted cells within target sites. In this study, thermosensitive chitosan chloride (CSCl) hydrogel was explored as injectable scaffold for adipose-derived MSCs (ADMSCs) delivery into ischemia/reperfusion (I/R) induced acute kidney injury (AKI). Thermosensitive CSCl hydrogels with/without ADMSCs were injected into the I/R site of rat AKI models. Dihydroethidium staining was used to detect the number of ROS in vivo. In order to track ADMSCs in vivo, ADMSCs were transfected with firefly luciferase and monomeric red fluorescent protein reporter genes (fluc-mrfp). The retention and survival of ADMSC were assessed using bioluminescence imaging, differentiation behaviors of ADMSCs were investigated using immunofluorescent and immunohistochemical staining. Proliferation and apoptosis of host renal cell in vivo were characterized by PCNA and TUNEL staining. Results suggested that CSCl hydrogels could improve the retention and survival of grafted ADMSCs, moreover, CSCl hydrogels could enhance the proliferation activity and reduce apoptosis of host renal cells. At 4 weeks, significant improvement of the renal function, microvessel density and tubular cell proliferation were observed in CSCl hydrogels with ADMSCs groups. Therefore, the application of thermosensitive CSCl hydrogel as scaffold for ADMSCs delivery into renal region could resolve the main obstacle of cell transplantation for acute kidney injury (AKI). Therefore, CSCl hydrogel is a potential cell carrier for treatment of AKI.