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Cisplatin-Induced Nephrotoxicity and...

Ighofose, Eloho,

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Cisplatin-Induced Nephrotoxicity and Adaptive Responses in Renal Progenitor Cells: Molecular Insights From Transcriptomic and Proteomic Analyses /

Record Type:	Electronic resources : Monograph/item
Title/Author:	Cisplatin-Induced Nephrotoxicity and Adaptive Responses in Renal Progenitor Cells: Molecular Insights From Transcriptomic and Proteomic Analyses // Eloho Ighofose.
Author:	Ighofose, Eloho,
Description:	1 electronic resource (144 pages)
Notes:	Source: Dissertations Abstracts International, Volume: 86-12, Section: B.
Contained By:	Dissertations Abstracts International86-12B.
Subject:	Cellular biology. -
Online resource:	https://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=31998000
ISBN:	9798280719071

Cisplatin-Induced Nephrotoxicity and Adaptive Responses in Renal Progenitor Cells: Molecular Insights From Transcriptomic and Proteomic Analyses /
Ighofose, Eloho,

Cisplatin-Induced Nephrotoxicity and Adaptive Responses in Renal Progenitor Cells: Molecular Insights From Transcriptomic and Proteomic Analyses /Eloho Ighofose. - 1 electronic resource (144 pages)

Source: Dissertations Abstracts International, Volume: 86-12, Section: B.

Cisplatin is a widely used chemotherapeutic agent known for its efficacy against various solid tumors, but its clinical utility is limited by dose-dependent nephrotoxicity. The renal proximal tubule, particularly its epithelial cell population, is highly susceptible to cisplatin-induced injury due to its role in solute transport and high metabolic activity. Recent advances suggest that renal progenitor cells play a key role in epithelial repair following nephrotoxic injury; however, the molecular mechanisms underlying their response to cisplatin remain poorly understood.This study investigates the impact of both acute and chronic cisplatin exposure on immortalized human renal progenitor cells (HRTPT, CD24⁺/CD133⁺) using a combination of transcriptomic (RNA sequencing) and proteomic (TMT-labeled mass spectrometry) approaches. Morphological changes and platinum accumulation were evaluated using microscopy and ICP-MS, respectively. RNA-seq data revealed progressive transcriptional reprogramming across passages, marked by the upregulation of DNA damage response, oxidative stress, and apoptosis pathways, alongside suppression of metabolic and transport-related genes. Proteomic analyses supported these findings, highlighting alterations in mitochondrial function and inflammatory signaling. Notably, partial discordance between transcript and protein levels suggested possible post-transcriptional regulation during cisplatin adaptation.The results demonstrate that HRTPT cells exhibit adaptive molecular responses to cisplatin-induced stress, including changes in gene expression, protein regulation, and cellular phenotype. These findings enhance our understanding of renal progenitor cell-mediated repair mechanisms and offer potential targets for therapeutic intervention to mitigate cisplatin nephrotoxicity. This study also validates HRTPT cells as a physiologically relevant in vitro model for studying nephrotoxic injury and regeneration in the human kidney.

English

ISBN: 9798280719071Subjects--Topical Terms:

3172791
Cellular biology.
Subjects--Index Terms:

Cisplatin

Cisplatin-Induced Nephrotoxicity and Adaptive Responses in Renal Progenitor Cells: Molecular Insights From Transcriptomic and Proteomic Analyses /
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520 $a Cisplatin is a widely used chemotherapeutic agent known for its efficacy against various solid tumors, but its clinical utility is limited by dose-dependent nephrotoxicity. The renal proximal tubule, particularly its epithelial cell population, is highly susceptible to cisplatin-induced injury due to its role in solute transport and high metabolic activity. Recent advances suggest that renal progenitor cells play a key role in epithelial repair following nephrotoxic injury; however, the molecular mechanisms underlying their response to cisplatin remain poorly understood.This study investigates the impact of both acute and chronic cisplatin exposure on immortalized human renal progenitor cells (HRTPT, CD24⁺/CD133⁺) using a combination of transcriptomic (RNA sequencing) and proteomic (TMT-labeled mass spectrometry) approaches. Morphological changes and platinum accumulation were evaluated using microscopy and ICP-MS, respectively. RNA-seq data revealed progressive transcriptional reprogramming across passages, marked by the upregulation of DNA damage response, oxidative stress, and apoptosis pathways, alongside suppression of metabolic and transport-related genes. Proteomic analyses supported these findings, highlighting alterations in mitochondrial function and inflammatory signaling. Notably, partial discordance between transcript and protein levels suggested possible post-transcriptional regulation during cisplatin adaptation.The results demonstrate that HRTPT cells exhibit adaptive molecular responses to cisplatin-induced stress, including changes in gene expression, protein regulation, and cellular phenotype. These findings enhance our understanding of renal progenitor cell-mediated repair mechanisms and offer potential targets for therapeutic intervention to mitigate cisplatin nephrotoxicity. This study also validates HRTPT cells as a physiologically relevant in vitro model for studying nephrotoxic injury and regeneration in the human kidney.
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650 4 $a Toxicology. $3 556884
650 4 $a Molecular biology. $3 517296
650 4 $a Genetics. $3 530508
650 4 $a Morphology. $3 591167
653 $a Cisplatin
653 $a Human renal progenitor cells
653 $a RNA sequencing
653 $a Cellular phenotype
653 $a Human kidney
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690 $a 0287
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