The Effect of Low-Power Laser Therapy on the TGF/β Signaling Pathway in Chronic Kidney Disease: A Review

Objective: The purpose of this study is to investigate the effects of low-power lasers on kidney disease by investigating several studies.Methods: A number of articles from 1998 to 2019 were chosen from the sources of PubMed, Scopus, and only the articles studying the effect of low-power lasers on kidney disease were investigated.Results: After reviewing the literature, 21 articles examining only the effects of low-power lasers on kidney disease were found. The results of these studies showed that the parameter of the low-power laser would result in different outcomes. So, a low-power laser with various parameters can be effective in the treatment of kidney diseases such as acute kidney disease, diabetes, glomerulonephritis, nephrectomy, metabolic syndrome, and kidney fibrosis. Most studies have shown that low-power lasers can affect TGFβ1 signaling which is the most important signaling in the treatment of renal fibrosis.Conclusion: Lasers can be effective in reducing or enhancing inflammatory responses, reducing fibrosis factors, and decreasing reactive oxygen species (ROS) levels in kidney disease and glomerular cell proliferation

Human Amniotic Membrane as a Suitable Matrix for Growth of Mouse Urothelial Cells in Comparison With Human Peritoneal and Omentum Membranes

Normal 0 false false false EN-US X-NONE AR-SA MicrosoftInternetExplorer4 /* Style Definitions */ table.MsoNormalTable {mso-style-name:"Table Normal"; mso-tstyle-rowband-size:0; mso-tstyle-colband-size:0; mso-style-noshow:yes; mso-style-priority:99; mso-style-qformat:yes; mso-style-parent:""; mso-padding-alt:0cm 5.4pt 0cm 5.4pt; mso-para-margin:0cm; mso-para-margin-bottom:.0001pt; mso-pagination:widow-orphan; font-size:11.0pt; font-family:"Calibri","sans-serif"; mso-ascii-font-family:Calibri; mso-ascii-theme-font:minor-latin; mso-fareast-font-family:"Times New Roman"; mso-fareast-theme-font:minor-fareast; mso-hansi-font-family:Calibri; mso-hansi-theme-font:minor-latin; mso-bidi-font-family:Arial; mso-bidi-theme-font:minor-bidi;} Introduction: For tissue engineering of the urinary tract system, cell culture requires to be established in vitro and an appropriate matrix acting as cell carrier should be developed. The aim of the present study was to assess the proliferation quality of mouse urothelial cells on 3 natural matrixes of human amniotic membrane (AM), peritoneum, and omentum, and to compare them with collagen matrix. Materials and Methods: Mouse urothelial cells were isolated by collagenase IV, and the urothelial cells (105 cells per milliliter) were cultured on the AM, peritoneum, omentum, and collagen. The pattern of growth and asymmetric unit membrane formation were analyzed by histologic examination and immunocytochemistry on the detached urothelium with pancytokeratin and uroplakin III, respectively. Electron micrographs were taken and cell layers, organelles, desmosomes, and junctions were studied. Results: Immunocytochemistry of cultivated cells confirmed the urothelial cells phenotype. Up to 4 cell layers were obtained on the AM and 1 to 2 layers on the peritoneum. Distribution of the urothelial cells on the omentum was not favorable, which was due to its large pores. Cell proliferation started later on the AM (7th day) compared to collagen (3rd day). Also, apoptosis started later on the AM (after 14 days) compared to collagen (7 days). Conclusion: These results showed that the AM can act as a cell carrier for culture of the urothelial cells, and its exceptional properties such as having various growth factors, availability, and cost-effectiveness make it a unique biological matrix for urothelial culture.</p

Potential of Autologous Adipose-Derived Mesenchymal Stem Cells in Peritoneal Fibrosis:A Pilot Study

Background: We aimed to determine the effects of systemic therapy with autologous adipose tissue derived mesenchymal stem cells (AD-MSCs) on different parameters of peritoneal function and inflammation in peritoneal dialysis (PD) patients.Methods: We enrolled nine PD patients with ultrafiltration failure (UFF). Patients received 1.2 &amp; PLUSMN; 0.1 x 106 cell/kg of AD-MSCs via cubital vein and were then followed for six months at time points of baseline, 3, 6, 12, 16 and 24 weeks after infusion. UNI-PET was performed for assessment of peritoneal characteristics at baseline and weeks 12 and 24. Systemic and peritoneal levels of tumor necrosis factor &amp; alpha; (TNF-&amp; alpha;), interleukin-6 (IL-6), IL-2 and CA125 (by ELISA) and gene expression levels of transforming growth factor beta (TGF-8), smooth muscle actin (&amp;#xfffd;&amp;#xfffd;&amp;#xfffd;&amp;#xfffd;&amp;#xfffd;&amp;#xfffd;-SMA) and fibroblast-specific protein-1 (FSP-1) in PD effluent derived cells (by quantitative real-time PCR) were measured at baseline and weeks 3, 6, 12, 16 and 24.Results: Slight improvement was observed in the following UF capacity indices: free water transport (FWT, 32%), ultrafiltration -small pore (UFSP, 18%), ultrafiltration total (UFT, 25%), osmotic conductance to glucose (OCG, 25%), D/P creatinine (0.75 to 0.70), and Dt/D0 glucose (0.23 to 0.26). There was a slight increase in systemic and peritoneal levels of CA125 and a slight decrease in gene expression levels of TGF-8, &amp; alpha;-SMA and FSP-1 that was more prominent at week 12 and vanished by the end of the study. Conclusion: Our results for the first time showed the potential of MSCs for treatment of peritoneal damage in a clinical trial. Our results could be regarded as hypothesis suggestion and will need confirmation in future studies

Identification of Three Novel Frameshift Mutations in the PKD1 Gene in Iranian Families with Autosomal Dominant Polycystic Kidney Disease Using Efficient Targeted Next-Generation Sequencing

Background/Aims: Autosomal dominant polycystic kidney disease (ADPKD) is one of the most common inherited cystic kidney diseases caused by mutations in two large multi-exon genes, PKD1 and PKD2. High allelic heterogeneity and duplication of PKD1 exons 1–32 as six pseudo genes on chromosome 16 complicate molecular analysis of this disease. Methods: We applied targeted next-generation sequencing (NGS) in 9 non-consanguineous unrelated Iranian families with ADPKD to identify the genes hosting disease-causing mutations. This approach was confirmed by Sanger sequencing. Results: Here, we determined three different novel frameshift mutations and four previously reported nonsense mutations in the PKD1 gene encoding polycystin1 in heterozygotes. Conclusion: This study demonstrates the effectiveness of NGS in significantly reducing the cost and time for simultaneous sequence analysis of PKD1 and PKD2, simplifying the genetic diagnostics of ADPKD. Although a probable correlation between the mutation types and phenotypic outcome is possible, however for more extensive studies in future, the consideration of renal hypouricemia (RHUC) and PKD1 coexistence may be helpful. The novel frameshift mutations reported by this study are p. Q1997X, P. D73X and p. V336X

Systemic Infusion of Autologous Adipose Tissue-Derived Mesenchymal Stem Cells in Peritoneal Dialysis Patients: Feasibility and Safety

Using mesenchymal stem cells (MSCs) is regarded as a new therapeutic approach for improving fibrotic diseases. The aim of this study to evaluate the feasibility and safety of systemic infusion of autologous adipose tissue-derived MSCs (AD-MSCs) in peritoneal dialysis (PD) patients with expected peritoneal fibrosis. Materials and Methods: This study was a prospective, open-label, non-randomized, placebo-free, phase I clinical trial. Case group consisted of nine eligible renal failure patients with more than two years of history of being on PD. Autologous AD-MSCs were obtained through lipoaspiration and expanded under good manufacturing practice conditions. Patients received 1.2 ± 0.1×106 cell/kg of AD-MSCs via cubital vein and then were followed for six months at time points of baseline, and then 3 weeks, 6 weeks, 12 weeks, 16 weeks and 24 weeks after infusion. Clinical, biochemical and peritoneal equilibration test (PET) were performed to assess the safety and probable change in peritoneal solute transport parameters. Results: No serious adverse events and no catheter-related complications were found in the participants. 14 minor reported adverse events were self-limited or subsided after supportive treatment. One patient developed an episode of peritonitis and another patient experienced exit site infection, which did not appear to be related to the procedure. A significant decrease in the rate of solute transport across peritoneal membrane was detected by PET (D/P cr=0.77 vs. 0.73, P=0.02). Conclusion: This study, for the first time, showed the feasibility and safety of AD-MSCs in PD patients and the potentials for positive changes in solute transport. Further studies with larger samples, longer follow-up, and randomized blind control groups to elucidate the most effective route, frequency and dose of MSCs administration, are necessary (Registration Number: IRCT2015052415841N2)

Enriched human embryonic stem cells-derived CD133+, CD24+ renal progenitors engraft and restore function in a gentamicin-induced kidney injury in mice

Introduction: Acute kidney injury (AKI) is a common health problem that leads to high morbidity and potential mortality. The failure of conventional treatments to improve forms of this condition highlights the need for innovative and effective treatment approaches. Regenerative therapies with Renal Progenitor Cells (RPCs) have been proposed as a promising new strategy. A growing body of evidence suggests that progenitor cells differentiated from different sources, including human embryonic stem cells (hESCs), can effectively treat AKI. Methods: Here, we describe a method for generating RPCs and directed human Embryoid Bodies (EBs) towards CD133+CD24+ renal progenitor cells and evaluate their functional activity in alleviating AKI. Results: The obtained results show that hESCs-derived CD133+CD24+ RPCs can engraft into damaged renal tubules and restore renal function and structure in mice with gentamicin-induced kidney injury, and significantly decrease blood urea nitrogen levels, suppress oxidative stress and inflammation, and attenuate histopathological disturbances, including tubular necrosis, tubular dilation, urinary casts, and interstitial fibrosis. Conclusion: The results suggest that RPCs have a promising regenerative potential in improving renal disease and can lay the foundation for future cell therapy and disease modeling

Additional file 2: Figure S1. of Safety and tolerability of autologous bone marrow mesenchymal stromal cells in ADPKD patients

Characterization of the patients’ bone mesenchymal stromal cells (MSCs). (DOCX 781 kb