Bactericidal Activity of Renal Tubular Cells: The Putative Role of Human β-Defensins

2002 ◽  
Vol 10 (5-6) ◽  
pp. 332-337 ◽  
Author(s):  
Martin Nitschke ◽  
Sandra Wiehl ◽  
Patrick C. Baer ◽  
Burkhard Kreft
Keyword(s):  
Bactericidal Activity ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Putative Role ◽  
Renal Tubular

Hypoxia-inducible factor modulates tubular cell survival in cisplatin nephrotoxicity

2005 ◽  
Vol 289 (5) ◽  
pp. F1123-F1133 ◽  
Author(s):  
Tetsuhiro Tanaka ◽  
Ichiro Kojima ◽  
Takamoto Ohse ◽  
Reiko Inagi ◽  
Toshio Miyata ◽  
...  
Keyword(s):  
Mitochondrial Membrane ◽  
Functional Role ◽  
Hypoxia Inducible Factor ◽  
Tubular Cell ◽  
Apoptotic Cells ◽  
Outer Medulla ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Renal Tubular

Hypoxia-inducible factor (HIF)-1 is a transcription factor mediating cellular response to hypoxia. Although it is expressed in tubular cells of the ischemic kidney, its functional role is not fully clarified in the pathological context. In this study, we investigated a role of HIF in tubular cell apoptosis induced by cisplatin. HIF-1α was expressed in tubular cells in the outer medulla 3 days after cisplatin (6 mg/kg) administration. With the in vivo administration of cobalt to activate HIF, the number of apoptotic renal tubular cells became much smaller in the outer medulla, compared with the vehicle group. We also examined the functional role of HIF-1 in vitro using immortalized rat proximal tubular cells (IRPTC). In hypoxia, IRPTC that express dominant-negative (dn) HIF-1α showed impaired survival in cisplatin injury at variable doses (25–100 μM, 24 h), which was not obvious in normoxia. The observed difference in cell viability in hypoxia was associated with the increased number of apoptotic cells in dnHIF-1α clones (Hoechst 33258 staining). Studies on intracellular signaling revealed that the degree of cytochrome c release, dissipation of mitochondrial membrane potentials, and caspase-9 activity were all more prominent in dnHIF-1α clones than in control IRPTC, pointing to the accelerated signaling of mitochondrial pathways. We propose that HIF-1 mediates cytoprotection against cisplatin injury in hypoxic renal tubular cells, by reducing the number of apoptotic cells through stabilization of mitochondrial membrane integrity and suppression of apoptosis signaling. A possibility was suggested that activation of HIF-1 could be a new promising therapeutic target for hypoxic renal diseases.

scholarly journals Exosome production and its regulation of EGFR during wound healing in renal tubular cells

2017 ◽  
Vol 312 (6) ◽  
pp. F963-F970 ◽  
Author(s):  
Xiangjun Zhou ◽  
Wei Zhang ◽  
Qisheng Yao ◽  
Hao Zhang ◽  
Guie Dong ◽  
...  
Keyword(s):  
Wound Healing ◽  
Wound Repair ◽  
Renal Tubules ◽  
Egfr Signaling ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Egfr Activation ◽  
Renal Tubular ◽  
The Relationship

Kidney repair following injury involves the reconstitution of a structurally and functionally intact tubular epithelium. Growth factors and their receptors, such as EGFR, are important in the repair of renal tubules. Exosomes are cell-produced small (~100 nm in diameter) vesicles that contain and transfer proteins, lipids, RNAs, and DNAs between cells. In this study, we examined the relationship between exosome production and EGFR activation and the potential role of exosome in wound healing. EGFR activation occurred shortly after scratch wounding in renal tubular cells. Wound repair after scratching was significantly promoted by EGF and suppressed by EGFR inhibitor gefitinib. Interestingly, scratch wounding induced a significant increase of exosome production. The exosome production was decreased by EGF and increased by gefitinib, suggesting a suppressive role of EGFR signaling in exosome production. Conversely, inhibition of exosome release by GW4869 and manumycin A markedly increased EGFR activation and promoted wound healing. Moreover, exosomes derived from scratch-wounding cells could inhibit wound healing. Collectively, the results indicate that wound healing in renal tubular cells is associated with EGFR activation and exosome production. Although EGFR activation promotes wound healing, released exosomes may antagonize EGFR activation and wound healing.

Abstract P544: Osteopontin Deficiency Decreases Autophagy and Exacerbates Tubular Injury in Acute Kidney Injury Induced by Folic Acid

Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
Tomoaki Nagao ◽  
Takafumi Okura ◽  
Akiko Tanino ◽  
Ken-ichi Miyoshi ◽  
Masayoshi Kukida ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Folic Acid ◽  
Kidney Injury ◽  
Immunohistochemical Analysis ◽  
Tubular Injury ◽  
Histological Changes ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Renal Tubular

Osteopontin (OPN), a secreted glycosylated phosphoprotein and pro-inflammatory cytokine, has been implicated in the pathology of several renal conditions, especially renal fibrosis in chronic kidney disease. OPN is slightly expressed in renal tubular cells in normal condition, but after acute tubular injury, OPN is highly induced in these cells. However, the role of induced OPN is still unclear. The aim of this study was to clarify the roles of OPN in acute kidney injury (AKI). AKI was induced in wild type (WT) and OPN knockout (KO) mice by using folic acid (FA) injection (0.35mg/kg). After 2days of injection, 34% of WT mice died, whereas 54% of KO died from renal failure. Kidneys from survived mice were removed and the renal histological changes, protein expression were examined. BUN and Creatinine levels were markedly elevated in WT-AKI and KO-AKI mice (BUN: WT-sham; 25.7±4.7mg/dl, WT-AKI; 315.0±173.2mg/dl, KO-AKI; 337.7±163.7mg/dl, Creatinine: WT-sham; 0.08±0.03 mg/dl, WT-AKI; 1.60±0.87 mg/dl, KO-AKI; 1.80±0.94 mg/dl). Renal OPN mRNA expression was increased in WT-AKI mice compared to WT-sham mice (p<0.05). High levels of OPN expression in renal tubular cells were induced in WT-AKI mice. TUNEL positive tubular cells were increased in KO-AKI mice compared to WT-AKI mice. In immunohistochemical analysis, Kidney injury molecules 1 (Kim-1) positive tubular cells were also highly increased in KO-AKI mice compared to WT-AKI mice. In contrast, LC3B (autophagy related protein) positive tubular cells were decreased in KO-AKI mice compared to WT-AKI mice. These results indicate that OPN deficiency exacerbates tubular injury via through the inhibiting autophagy in folic acid induced AKI mice.

The Role of Growth Factors on Renal Tubular Cells Submitted to Hypoxia and Deprived of Glucose

Renal Failure ◽  
2003 ◽  
Vol 25 (3) ◽  
pp. 341-353 ◽  
Author(s):  
Marcelino de Souza Durão ◽  
Clara Versolato Razvickas ◽  
Elsa Alídia Petry Gonçalves ◽  
Iria Ruriko Okano R.N. ◽  
Simone Mafalda Rodrigues Camargo ◽  
...  
Keyword(s):  
Growth Factors ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Renal Tubular

New role of the human equilibrative nucleoside transporter 1 (hENT1) in Epithelial-to-mesenchymal transition in renal tubular cells

2012 ◽  
Vol 227 (4) ◽  
pp. 1521-1528 ◽  
Author(s):  
Elena Guillén-Gómez ◽  
Itziar Pinilla-Macua ◽  
Sandra Pérez-Torras ◽  
Doo-Sup Choi ◽  
Yolanda Arce ◽  
...  
Keyword(s):  
Epithelial To Mesenchymal Transition ◽  
Nucleoside Transporter ◽  
Mesenchymal Transition ◽  
Equilibrative Nucleoside Transporter ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Renal Tubular

scholarly journals Radiocontrast-induced DNA fragmentation of renal tubular cells in vitro: role of hypertonicity

1998 ◽  
Vol 13 (4) ◽  
pp. 911-918 ◽  
Author(s):  
I. Hizoh ◽  
J. Strater ◽  
C. Schick ◽  
W. Kubler ◽  
C. Haller
Keyword(s):  
Dna Fragmentation ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Renal Tubular

scholarly journals An interplay between UCP2 and ROS protects cells from high-salt-induced injury through autophagy stimulation

2021 ◽  
Vol 12 (10) ◽  
Author(s):  
Maurizio Forte ◽  
Franca Bianchi ◽  
Maria Cotugno ◽  
Simona Marchitti ◽  
Rosita Stanzione ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Animal Models ◽  
High Salt ◽  
Autophagic Flux ◽  
Protective Function ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Ros Accumulation ◽  
Renal Tubular

AbstractThe mitochondrial uncoupling protein 2 (UCP2) plays a protective function in the vascular disease of both animal models and humans. UCP2 downregulation upon high-salt feeding favors vascular dysfunction in knock-out mice, and accelerates cerebrovascular and renal damage in the stroke-prone spontaneously hypertensive rat. Overexpression of UCP2 counteracts the negative effects of high-salt feeding in both animal models. We tested in vitro the ability of UCP2 to stimulate autophagy and mitophagy as a mechanism mediating its protective effects upon high-salt exposure in endothelial and renal tubular cells. UCP2 silencing reduced autophagy and mitophagy, whereas the opposite was true upon UCP2 overexpression. High-salt exposure increased level of reactive oxygen species (ROS), UCP2, autophagy and autophagic flux in both endothelial and renal tubular cells. In contrast, high-salt was unable to induce autophagy and autophagic flux in UCP2-silenced cells, concomitantly with excessive ROS accumulation. The addition of an autophagy inducer, Tat-Beclin 1, rescued the viability of UCP2-silenced cells even when exposed to high-salt. In summary, UCP2 mediated the interaction between high-salt-induced oxidative stress and autophagy to preserve viability of both endothelial and renal tubular cells. In the presence of excessive ROS accumulation (achieved upon UCP2 silencing and high-salt exposure of silenced cells) autophagy was turned off. In this condition, an exogenous autophagy inducer rescued the cellular damage induced by excess ROS level. Our data confirm the protective role of UCP2 toward high-salt-induced vascular and renal injury, and they underscore the role of autophagy/mitophagy as a mechanism counteracting the high-salt-induced oxidative stress damage.

Sign in / Sign up

Export Citation Format

Share Document