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- 저자 : Babu J. Padanilam (검색결과 5 건)
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Babu J. Padanilam 대한신장학회 2017 Kidney Research and Clinical Practice Vol.36 No.4
Fibrosis is the hallmark of end-stage organ disease and accounts for 45% of deaths around the world. Fibrosis is a key component in the progression of chronic kidney disease and involves the activation and accumulation of fibroblasts or myofibroblasts and the deposition of an extracellular matrix. Although it was previously thought that all collagen-producing fibroblasts originated solely from resident fibroblasts, other important sources of fibroblasts have been proposed, such as pericytes, circulating fibrocytes of bone marrow origin, and fibroblasts that originate from epithelial mesenchymal transition (EMT) and endothelial mesenchymal transition (EndMT) [1]. However, the contribution of these different sources to myofibroblast formation is under debate, and no consensus has been reached, particularly with respect to EMT and EndMT [1].
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Daeun Moon,Babu J. Padanilam,Hee-Seong Jang,Jinu Kim 대한체질인류학회 2020 해부·생물인류학 (Anat Biol Anthropol) Vol.33 No.4
Calcitonin gene-related peptide (CGRP) derived from sensory neurons contributes to the development of renal tubulointerstitial fibrosis during ureteral obstruction through upregulation of profibrotic factors. However, the mechanism by which CGRP upregulates the profibrotic factors in the ureteral obstructive setting in the kidney tubule epithelial cells is not defined. In the human kidney proximal tubule epithelial cell line, HK-2, treatment with 1 nM CGRP significantly enhanced transforming growth factor-β1 (TGF-β1) production, its release, and protein kinase C (PKC) activity. Furthermore, mechanical stretch for 6 and 24 hours significantly increased expressions of receptor activity modifying protein 1 (RAMP1) mRNA and protein among CGRP receptor components in HK-2 cells. In addition, a combination treatment with CGRP and mechanical stretch synergistically increased TGF-β1 upregulation and PKC activation. However, RAMP1 deficiency, induced by RAMP1 double nickase plasmid transfection, abolished CGRP-induced TGF-β1 upregulation and PKC activation in HK-2 cells with or without mechanical stretch. Finally, pharmacological inhibition of PKC markedly reduced TGF-β1 production and release after treatment of HK-2 cells with CGRP. Taken together, these data suggest that extraneural CGRP upregulates TGF-β1 through RAMP1-PKC axis during mechanical stretch in kidney proximal tubule epithelial cells.
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Mitochondrial fatty acid metabolism in acute kidney injury
Jang, Hee-Seong,Padanilam, Babu J. Institute for Medical Science 2018 The Journal of Medicine and Life Science Vol.15 No.2
Mitochondrial injury in renal tubule has been recognized as a major contributor in acute kidney injury (AKI) pathogenesis. Ischemic insult, nephrotoxin, endotoxin and contrast medium destroy mitochondrial structure and function as well as their biogenesis and dynamics, especially in renal proximal tubule, to elicit ATP depletion. Mitochondrial fatty acid ${\beta}$-oxidation (FAO) is the preferred source of ATP in the kidney, and its impairment is a critical factor in AKI pathogenesis. This review explores current knowledge of mitochondrial dysfunction and energy depletion in AKI and prospective views on developing therapeutic strategies targeting mitochondrial dysfunction in AKI.
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( Hee-seong Jang ),( Jinu Kim ),( Babu J. Padanilam ) 대한신장학회 2019 Kidney Research and Clinical Practice Vol.38 No.1
Chronic kidney disease (CKD) is increasing worldwide without an effective therapeutic strategy. Sympathetic nerve activation is implicated in CKD progression, as well as cardiovascular dysfunction. Renal denervation is beneficial for controlling blood pressure (BP) and improving renal function through reduction of sympathetic nerve activity in patients with resistant hypertension and CKD. Sympathetic neurotransmitter norepinephrine (NE) via adrenergic receptor (AR) signaling has been implicated in tissue homeostasis and various disease progressions, including CKD. Increased plasma NE level is a predictor of survival and the incidence of cardiovascular events in patients with endstage renal disease, as well as future renal injury in subjects with normal BP and renal function. Our recent data demonstrate that NE derived from renal nerves causes renal inflammation and fibrosis progression through alpha-2 adrenergic receptors (α<sub>2</sub>-AR) in renal fibrosis models independent of BP. Sympathetic nerve activation-associated molecular mechanisms and signals seem to be critical for the development and progression of CKD, but the exact role of sympathetic nerve activation in CKD progression remains undefined. This review explores the current knowledge of NE-α<sub>2</sub>-AR signaling in renal diseases and offers prospective views on developing therapeutic strategies targeting NE-AR signaling in CKD progression.
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Extraneural CGRP Induces Oxidative Stress in Kidney Proximal Tubule Epithelial Cells
문다은,윤상필,장희성,Mi Ra Noh,Ligyeom Ha,Babu J. Padanilam,김진우 대한체질인류학회 2019 대한체질인류학회지 Vol.32 No.4
Calcitonin gene-related peptide (CGRP) is the most abundant neuropeptide in primary afferent sensory neurons. Exogenous CGRP can induce cell death in kidney tubular cells. The objective of this study was to determine whether exogenous CGRP could induce reactive oxygen species (ROS) production in kidney proximal tubule epithelial cells and whether CGRP-induced ROS production might contribute to cell death. In HK-2, LLCPK1 and TCMK-1 cell lines derived from human, pig, and mouse respectively, administration of CGRP increased cell death in time- and dose-dependent manners, as demonstrated by decreased cell viability. Exogenous CGRP also increased ROS production levels in those cell lines. Treatment with CGRP receptor antagonist (CGRP8-37) significantly inhibited the increases in cell death and ROS production in CGRP-exposed cells. Furthermore, treatment with a ROS scavenger (MnTMPyP) markedly reduced kidney proximal tubule epithelial cell death after CGRP administration. Taken together, these data suggest that extraneural CGRP can induce cell death through excessive oxidative stress in kidney proximal tubule epithelial cells.
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