Apoptosis by Cyclosporine in Mesangial Cells

Han, Seongwoo; Chang, Eun‐Ju; Choi, Hee Joung; Kwak, Chun-Sik; Park, S.B.; Kim, H.C.; Mun, Kyo‐Cheol

doi:10.1016/j.transproceed.2006.06.029

Cited by 20 publications

(15 citation statements)

References 11 publications

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“…This finding was in agreement with Han et al (2006) who observed the presence of an increase in apoptotic cells in close association with the pathologic signs of CsA tubulo-interstitial damage. They attributed this fact to increase of expression in specific apoptotic genes.…”

Section: Discussionsupporting

confidence: 93%

“…Ying et al (2003) stated that patients must take this drug over their lifetime. Previous studies reported that a major limiting factor in the clinical use of CsA is chronic nephrotoxicity (Amore et al 2000;Han et al 2006). Zhong et al (2001) and Tirkey et al (2005) suggested a role for reactive oxygen metabolites as one of the postulated mechanisms in the pathogenesis of cyclosporine nephrotoxicity.…”

Section: Introductionmentioning

confidence: 99%

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Prophylactic role of curcumin against cyclosporine-induced nephrotoxicity: Histological and immunohistological study

Fattah

He²,

Fa³

et al. 2010

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Abstract. This study aimed to investigate the possible protective role of curcumin against renal damage caused by administration of cyclosporine A (CsA) in adult male rats. For this purpose, 27 adult male albino rats were used and divided into three equal groups. Group I (control group) and group II (CsA-treated group) received a daily subcutaneous injection of CsA at a dose of 20 mg/kg b.w. Group III (prophylactic group) received a daily oral curcumin at a dose of 15 mg/kg b.w. simultaneously with CsA. After 21 days, all the animals were anaesthetized and the kidneys were rapidly removed and processed to prepare paraffin sections stained with H&E, PAS and Masson's trichrome. In addition, the glutathione S-transferase (GST) enzyme was detected immunohistochemically. The optical density and the area (in %) of positive GST immunoreactions were measured in the cytoplasm of renal tubules and glomeruli and the data were statistically analyzed. Examination of sections from CsA-treated group showed renal tubules with vacuolated cytoplasm and others with darkly stained pyknotic nuclei. Apical brush borders of proximal tubules were undefined and PAS positive granules were noticed in their cytoplasm. The renal corpuscles contained shrunken glomeruli with widening of their Bowman's spaces. Inflammatory cellular infiltrate and increase in the collagen fibers were observed between the renal tubules. In prophylactic group, the structure of renal tubules and corpuscles were preserved except few tubular darkly stained pyknotic nuclei. Numerous blood vessels, few cellular infiltration and thin collagen fibers were observed between the renal tubules. Statistical analysis of morphometric data showed significant increase in the optical density of GST immunoreactivity in the cells of renal tubules and glomeruli of CsAtreated group when compared with the control or prophylactic groups. However, a significant decrease in the area of GST immunoreactivity in sections from prophylactic group was observed when compared with control or CsA-treated groups. In conclusion, protective effect of curcumin against cyclosporine-induced nephrotoxicity in rats was proven based on the study of histological changes and GST immunoexpression. This study supposes the possible therapeutic applications of curcumin in CsA-treated patients.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Prophylactic role of curcumin against cyclosporine-induced nephrotoxicity: Histological and immunohistological study

Fattah

He²,

Fa³

et al. 2010

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“…The present study confirmed that LPS can induce caspase-3-mediated apoptosis in kidney cells originating from the distal convoluted tubules. Previous in vitro experiments have also established that renal epithelial cells exposed to various chemical agents (staurosporine [10], TNFα [3], cyclosporine [10,21], antitumor platinum derivatives [22][23][24][25], cadmium [26][27][28][29],or even during pathological situations (ischemia/reperfusion, [30]) are dying through apoptotic processes.…”

Section: Discussionmentioning

confidence: 99%

KCNQ1 K<sup>+</sup> Channels are Involved in Lipopolysaccharide-induced Apoptosis of Distal Kidney Cells

Duranton¹,

Rubera²,

L’Hoste³

et al. 2010

Cell Physiol Biochem

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Most bacteria initiate host inflammatory responses through interactions with epithelial cells. Lipopolysaccharide (LPS), a component of the bacterial cell wall is a major cause of septic shock in emergency care units and in the pathogenesis of acute renal failure. Kidney cells exposed to LPS undergo apoptotic changes, including cell volume decrease, phosphatidylserine exposure, caspase-3- and membrane K⁺ conductance -activation. Whole-cell configuration was used to identify K⁺ channels in primary and immortalized culture of mice distal convoluted tubules. LPS exposure induced a 3 fold increase in intracellular cAMP concentration and the activation of an outwardly rectifying K⁺ conductance in both immortalized and primary culture of distal cells. This LPS-induced current exhibited KCNQ1 K⁺ channel characteristics, i.e. inhibition by quinidine, chromanol293B and low dose of HMR1556 (IC50<1 µM) and insensitive to TEA and charybdotoxin. The background-like biophysical properties of the current suggest that the KCNQ1 pore-forming subunit is associated with a KCNE2 or KCNE3 ancillary subunit. RT-PCR experiments confirmed the presence of KCNQ1 and KCNE3 mRNA transcripts in primary culture of distal segments. Activation of the KCNQ1/KCNE3 K⁺ current appeared to be an essential step in the LPS-induced apoptosis process since HMR1556 blocked the LPS-induced- cell volume decrease, -caspase-3 activation and -phosphatidylserine exposure.

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“…P53 was upregulated and activated in the renal cortex of db/db mice and streptozotocin (STZ)-induced diabetic mice and rats, leading to the increased podocyte apoptosis and albuminuria (53,54). In addition, p53 could also increase the apoptosis of mesangial cells and tubular cells, resulting in the aggravation of kidney damage (43,54,55). Furthermore, deletion of the p53 gene or inhibition of p53 protein function by its inhibitor conferred a protective phenotype because of the reduced apoptosis of renal cells (53,54).…”

Section: Sirt1 Inhibits Apoptosis By Targeting P53 Smad7 Foxo3 and mentioning

confidence: 99%

Sirtuin 1: A Target for Kidney Diseases

Kong

Zhou

et al. 2015

Mol Med

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Sirtuin 1 (SIRT1) is an evolutionarily conserved NAD + -dependent histone deacetylase that is necessary for caloric restriction-related lifespan extension. SIRT1, as an intracellular energy sensor, detects the concentration of intracellular NAD + and uses this information to adapt cellular energy output to cellular energy requirements. Previous studies on SIRT1 have confirmed its beneficial effects on cellular immunity to oxidative stress, reduction of fibrosis, suppression of inflammation, inhibition of apoptosis, regulation of metabolism, induction of autophagy and regulation of blood pressure. All of the above biological processes are involved in the pathogenesis of kidney diseases. Therefore, the activation of SIRT1 may become a therapeutic target to improve the clinical outcome of kidney diseases. In this review, we give an overview of SIRT1 and its molecular targets as well as SIRT1-modulated biological processes, with a particular focus on the role of SIRT1 in kidney diseases.

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Apoptosis by Cyclosporine in Mesangial Cells

Cited by 20 publications

References 11 publications

Prophylactic role of curcumin against cyclosporine-induced nephrotoxicity: Histological and immunohistological study

Prophylactic role of curcumin against cyclosporine-induced nephrotoxicity: Histological and immunohistological study

KCNQ1 K<sup>+</sup> Channels are Involved in Lipopolysaccharide-induced Apoptosis of Distal Kidney Cells

Sirtuin 1: A Target for Kidney Diseases

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