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Human Renal Epithelial Cells
Cat.No.: CSC-C1560
Species: Human
Source: Kidney
Cell Type: Epithelial
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HREpiC are isolated from human kidneys. HREpiC are cryopreserved at passage one and delivered frozen. Each vial contains >5 x 10^5 cells in 1 ml volume. HREpiC are characterized by immunofluorescent method with antibodies to cytokeratin-18, -19 and vimentin. HREpiC are negative for HIV-1, HBV, HCV, mycoplasma, bacteria, yeast and fungi. HREpiC are guaranteed to further expand for 15 population doublings in the condition provided by Creative Bioarray.
Human renal epithelial cells, essential to kidney function, constitute the epithelial tissue within the organ. They can be categorized into three primary types based on their location. The first type is simple squamous epithelial cells, primarily found within the glomerular vascular cavity, differentiated from mesenchymal cells. These cells maintain nephron filtration and stabilize the glomerular microenvironment. The second type is renal cuboidal epithelial cells, or renal tubular epithelial cells. Spread throughout the renal tubule interstitium, these cells are subdivided into proximal tubular cells, distal tubular cells, and thin segment epithelial cells, depending on their location within the tubule. Lastly, simple columnar epithelial cells reside mainly in certain parts of the collecting ducts, such as the papillary ducts.
The kidneys' primary function is to filter blood, forming urine to eliminate metabolic waste and excess water. Renal epithelial cells play a critical role in this process. They also reabsorb essential nutrients like glucose and amino acids from primary urine and secrete hydrogen ions to regulate acid-base balance. Additionally, these cells have immune functions and can initiate inflammatory responses when the kidney is damaged or infected, secreting inflammatory mediators and recruiting immune cells for repair and defense.
Given their crucial role in kidney, renal tubular epithelial cells are pivotal in renal disease research, often used as in vitro models to simulate the renal microenvironment. These models help study cellular changes related to resorption, secretion, and excretion under specific conditions. Sensitive to drug toxicity, renal tubular epithelial cells are valuable for evaluating potential nephrotoxic effects of pharmaceuticals. Moreover, their role in renal fibrosis, particularly in promoting interstitial fibrosis through cytokine release, is a key area of investigation.
Fig. 1. Typical renal tubular epithelial cells (Bhatnagar, R., Drachenberg, C., et al., 2014).
Losartan Mitigates Mechanotransduction Properties Alteration and EMT in Renal Epithelial Cells
he biological properties of kidney cells are constantly affected by biomechanical forces. Recent studies have demonstrated that biomechanical stimuli induce EMT through cytoskeletal rearrangements in renal epithelial cells. Angiotensin type 1 receptor (AT1R) activation has been widely recognized to stimulate pro-fibrotic effects, namely inflammatory cell recruitment, angiogenesis, cell proliferation, and ECM synthesis. Concurrently, angiotensin receptor blockers (ARBs) have been shown to improve or reverse fibrosis. However, it is still absence of consensus about the dose-dependency effect and precise mechanism of ARBs in mitigating renal fibrosis. Huang et al. hypothesize that a relatively lower dose of ARBs may also be beneficial of biomechanical stress-induced renal fibrosis.
Losartan, one of the most popularly used ARBs, even at a lower dose effectively alleviates the renal fibrosis in a unilateral ureteral obstruction (UUO) model of mice. They loaded human renal epithelial cells to a hydrostatic pressure of 50 mmHg in vitro to mimic the elevated intrarenal hydrostatic pressure in the UUO model. The immunofluorescence staining results showed a significant increase in the total expression of AT1R in renal epithelial cells (Fig. 1A). However, these changes were canceled by adding different concentrations of losartan, one of the most popularly used ARBs. The expression of F-actin displayed dense parallel networks and increased intensity in renal epithelial cells. These changes were almost canceled by losartan also (Fig. 1B). The protein level detection of EMT markers showed significant upregulation of vimentin, β-catenin, and a-SMA, but downregulation of E-cadherin in renal epithelial cells (Fig. 2). As expected, the addition of 10nM and 100nM losartan in the medium reduced the hydrostatic pressure-induced changes in EMT markers in renal epithelial cells (Fig. 2).
Fig. 1. Immunofluorescence staining on AT1R and F-actin in human renal epithelial cells (Huang Z., Nie H., et al., 2023).
Fig. 2. The expression of E-cadherin, β-catenin, vimentin and α-SMA in human renal epithelial cells (Huang Z., Nie H., et al., 2023).
Long-term HP Treatment Induced Severe Changes in Cell Morphology and Growth Factor Expression in HREpCs
Obstructive uropathy is a common kidney disease caused by elevated hydrostatic pressure (HP), but the molecular and cellular mechanisms have not been well understood. Chen et al. investigated how elevated HP affects the expression of growth factors in human renal epithelial cells (HREpC), providing new mechanistic insights into kidney injury induced by elevated HP.
After treating HREpC with HP for 48 hours, the cell morphology showed that some HREpC became rounded (Fig. 3A and B). The cell aspect ratio increased but returned to baseline levels within 72 hours after removing HP treatment, indicating that the elongation of HP-treated cells was reversible (Fig. 3C). MTT assay showed a slight decrease in cell viability in HP-treated cells compared to control cells (Fig. 3D). Furthermore, F-actin in HP-treated cells exhibited an elongated morphology (Fig. 3E). The growth factor expression results indicated that the expression of CSF2 and VEGFB was decreased in HP-treated cells after HP removal. The expression of TGFB2 and PDGFB decreased after long-term HP treatment and subsequent removal. Meanwhile, TGFB3 expression increased in HP-treated cells after HP removal. The expression of VEGFA decreased in HP-treated cells 72 hours after HP removal (Fig. 4).
Fig. 3. Long-term HP treatment induced severe changes in cell morphology and growth factor expression in HREpCs (Yan C., Xiao J. et al., 2024).
Fig. 4. The expression of growth factors in HREpCs received 100 cmH2O HP treatment for 48 h (Yan C., Xiao J. et al., 2024).
Human Renal Epithelial Cells from Creative Bioarray are comprised of cells from the cortex and glomerular region.
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