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Article: Editorial: Premature Aging and Senescence in Renal Fibrosis.

Samarakoon, Rohan / Higgins, Paul J

2021 Volume 12, Page(s) 734892

Language	English
Publishing date	2021-07-26
Publishing country	Switzerland
Document type	Editorial
ZDB-ID	2587355-6
ISSN	1663-9812
ISSN	1663-9812
DOI	10.3389/fphar.2021.734892
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Article: Downstream Targets of VHL/HIF-α Signaling in Renal Clear Cell Carcinoma Progression: Mechanisms and Therapeutic Relevance.

Mazumder, Sonia / Higgins, Paul J / Samarakoon, Rohan

Cancers

2023 Volume 15, Issue 4

Abstract: The clear cell variant of renal cell carcinoma (ccRCC) is the most common renal epithelial malignancy and responsible for most of the deaths from kidney cancer. Patients carrying inactivating mutations in the Von Hippel-Lindau (VHL) gene have an ... ...

Abstract	The clear cell variant of renal cell carcinoma (ccRCC) is the most common renal epithelial malignancy and responsible for most of the deaths from kidney cancer. Patients carrying inactivating mutations in the Von Hippel-Lindau (VHL) gene have an increased proclivity to develop several types of tumors including ccRCC. Normally, the Hypoxia Inducible Factor alpha (HIF-α) subunits of the HIF heterodimeric transcription factor complex are regulated by oxygen-dependent prolyl-hydroxylation, VHL-mediated ubiquitination and proteasomal degradation. Loss of pVHL function results in elevated levels of HIF-α due to increased stability, leading to RCC progression. While HIF-1α acts as a tumor suppressor, HIF-2α promotes oncogenic potential by driving tumor progression and metastasis through activation of hypoxia-sensitive signaling pathways and overexpression of HIF-2α target genes. One strategy to suppress ccRCC aggressiveness is directed at inhibition of HIF-2α and the associated molecular pathways leading to cell proliferation, angiogenesis, and metastasis. Indeed, clinical and pre-clinical data demonstrated the effectiveness of HIF-2α targeted therapy in attenuating ccRCC progression. This review focuses on the signaling pathways and the involved genes (cyclin D, c-Myc, VEGF-a, EGFR, TGF-α, GLUT-1) that confer oncogenic potential downstream of the VHL-HIF-2α signaling axis in ccRCC. Discussed as well are current treatment options (including receptor tyrosine kinase inhibitors such as sunitinib), the medical challenges (high prevalence of metastasis at the time of diagnosis, refractory nature of advanced disease to current treatment options), scientific challenges and future directions.
Language	English
Publishing date	2023-02-19
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers15041316
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Article ; Online: Mineralocorticoid Receptor-Associated Mechanisms in Diabetic Kidney Disease and Clinical Significance of Mineralocorticoid Receptor Antagonists.

Mende, Christian W / Samarakoon, Rohan / Higgins, Paul J

American journal of nephrology

2023 Volume 54, Issue 1-2, Page(s) 50–61

Abstract: Background: Diabetic kidney disease (DKD) is a common disorder with multiple serious clinical implications, including an increased risk of end-stage kidney disease (ESKD), cardiovascular complications, heart failure, onset or worsening of hypertension, ... ...

Abstract	Background: Diabetic kidney disease (DKD) is a common disorder with multiple serious clinical implications, including an increased risk of end-stage kidney disease (ESKD), cardiovascular complications, heart failure, onset or worsening of hypertension, and premature death. Patients with DKD frequently require dialysis or kidney transplantation to manage their ESKD. Summary: Upregulation of the renin-angiotensin-aldosterone system is an important contributor to kidney disease progression, as highlighted by the results of trials evaluating angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in patients with albuminuria. Increasing evidence suggests the existence of a multidirectional network that involves aldosterone, the mineralocorticoid receptor (MR), and the Ras-related C3 botulinum toxin substrate 1 (Rac1) as driving forces in the generation of reactive oxygen species and oxidative stress-induced injury in the initiation of interstitial nephritis and eventual fibrosis in chronic kidney disease and DKD. The MR is a key element of this triangle, as highlighted by the beneficial effect of MR antagonists in preventing or reducing aldosterone- or Rac1-related effects in basic science studies, and the improved patient outcomes observed in clinical studies. Key messages: Aldosterone can promote kidney disease in diabetes via the MR and via MR-independent actions through Rac1. However, the MR remains a key element of this triangle, with clinical data supporting the use of MR antagonists in delaying the progression of kidney disease in diabetes.
MeSH term(s)	Humans ; Mineralocorticoid Receptor Antagonists/adverse effects ; Diabetic Nephropathies/drug therapy ; Diabetic Nephropathies/etiology ; Aldosterone ; Receptors, Mineralocorticoid ; Clinical Relevance ; Kidney Failure, Chronic/drug therapy ; Angiotensin Receptor Antagonists/pharmacology ; Angiotensin Receptor Antagonists/therapeutic use ; Diabetes Mellitus
Chemical Substances	Mineralocorticoid Receptor Antagonists ; Aldosterone (4964P6T9RB) ; Receptors, Mineralocorticoid ; Angiotensin Receptor Antagonists
Language	English
Publishing date	2023-01-20
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	604540-6
ISSN	1421-9670 ; 0250-8095
ISSN (online)	1421-9670
ISSN	0250-8095
DOI	10.1159/000528783
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Article: Cancer-Associated Fibroblasts: Mechanisms of Tumor Progression and Novel Therapeutic Targets.

Czekay, Ralf-Peter / Cheon, Dong-Joo / Samarakoon, Rohan / Kutz, Stacie M / Higgins, Paul J

Cancers

2022 Volume 14, Issue 5

Abstract: Cancer-associated fibroblasts (CAFs) are a heterogenous population of stromal cells found in solid malignancies that coexist with the growing tumor mass and other immune/nonimmune cellular elements. In certain neoplasms (e.g., desmoplastic tumors), CAFs ... ...

Abstract	Cancer-associated fibroblasts (CAFs) are a heterogenous population of stromal cells found in solid malignancies that coexist with the growing tumor mass and other immune/nonimmune cellular elements. In certain neoplasms (e.g., desmoplastic tumors), CAFs are the prominent mesenchymal cell type in the tumor microenvironment, where their presence and abundance signal a poor prognosis in multiple cancers. CAFs play a major role in the progression of various malignancies by remodeling the supporting stromal matrix into a dense, fibrotic structure while secreting factors that lead to the acquisition of cancer stem-like characteristics and promoting tumor cell survival, reduced sensitivity to chemotherapeutics, aggressive growth and metastasis. Tumors with high stromal fibrotic signatures are more likely to be associated with drug resistance and eventual relapse. Clarifying the molecular basis for such multidirectional crosstalk among the various normal and neoplastic cell types present in the tumor microenvironment may yield novel targets and new opportunities for therapeutic intervention. This review highlights the most recent concepts regarding the complexity of CAF biology including CAF heterogeneity, functionality in drug resistance, contribution to a progressively fibrotic tumor stroma, the involved signaling pathways and the participating genes.
Language	English
Publishing date	2022-02-27
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers14051231
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Article ; Online: Potential renal stem/progenitor cells identified by in vivo lineage tracing.

Zhang, Wenzheng / Gao, Chao / Tsilosani, Akaki / Samarakoon, Rohan / Plews, Robert / Higgins, Paul J

American journal of physiology. Renal physiology

2022 Volume 322, Issue 4, Page(s) F379–F391

Abstract: Mammalian kidneys consist of more than 30 different types of cells. A challenging task is to identify and characterize the stem/progenitor subpopulations that establish the lineage relationships among these cellular elements during nephrogenesis in the ... ...

Abstract	Mammalian kidneys consist of more than 30 different types of cells. A challenging task is to identify and characterize the stem/progenitor subpopulations that establish the lineage relationships among these cellular elements during nephrogenesis in the embryonic and neonate kidneys and during tissue homeostasis and/or injury repair in the mature kidney. Moreover, the potential clinical utility of stem/progenitor cells holds promise for the development of new regenerative medicine approaches for the treatment of renal diseases. Stem cells are defined by unlimited self-renewal capacity and pluripotentiality. Progenitor cells have pluripotentiality but no or limited self-renewal potential. Cre-LoxP-based in vivo genetic lineage tracing is a powerful tool to identify stem/progenitor cells in their native environment. Hypothetically, this technique enables investigators to accurately track the progeny of a single cell or a group of cells. The Cre/LoxP system has been widely used to uncover the function of genes in various mammalian tissues and to identify stem/progenitor cells through in vivo lineage tracing analyses. In this review, we summarize the recent advances in the development and characterization of various Cre drivers and their use in identifying potential renal stem/progenitor cells in both developing and mature mouse kidneys.
MeSH term(s)	Animals ; Cell Differentiation ; Cell Lineage ; Homeostasis ; Kidney ; Mammals ; Mice ; Organogenesis ; Stem Cells
Language	English
Publishing date	2022-01-31
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural
ZDB-ID	603837-2
ISSN	1522-1466 ; 0363-6127
ISSN (online)	1522-1466
ISSN	0363-6127
DOI	10.1152/ajprenal.00326.2021
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Article ; Online: Emerging role of tumor suppressor p53 in acute and chronic kidney diseases.

Overstreet, Jessica M / Gifford, Cody C / Tang, Jiaqi / Higgins, Paul J / Samarakoon, Rohan

Cellular and molecular life sciences : CMLS

2022 Volume 79, Issue 9, Page(s) 474

Abstract: p53 is a major regulator of cell cycle arrest, apoptosis, and senescence. While involvement of p53 in tumorigenesis is well established, recent studies implicate p53 in the initiation and progression of several renal diseases, which is the focus of this ... ...

Abstract	p53 is a major regulator of cell cycle arrest, apoptosis, and senescence. While involvement of p53 in tumorigenesis is well established, recent studies implicate p53 in the initiation and progression of several renal diseases, which is the focus of this review. Ischemic-, aristolochic acid (AA) -, diabetic-, HIV-associated-, obstructive- and podocyte-induced nephropathies are accompanied by activation and/or elevated expression of p53. Studies utilizing chemical or renal-specific inhibition of p53 in mice confirm the pathogenic role of this transcription factor in acute kidney injury and chronic kidney disease. TGF-β1, NOX, ATM/ATR kinases, Cyclin G, HIPK, MDM2 and certain micro-RNAs are important determinants of renal p53 function in response to trauma. AA, cisplatin or TGF-β1-mediated ROS generation via NOXs promotes p53 phosphorylation and subsequent tubular dysfunction. p53-SMAD3 transcriptional cooperation downstream of TGF-β1 orchestrates induction of fibrotic factors, extracellular matrix accumulation and pathogenic renal cell communication. TGF-β1-induced micro-RNAs (such as mir-192) could facilitate p53 activation, leading to renal hypertrophy and matrix expansion in response to diabetic insults while AA-mediated mir-192 induction regulates p53 dependent epithelial G
MeSH term(s)	Animals ; Fibrosis ; Humans ; Kidney/metabolism ; Kidney Diseases/metabolism ; Mice ; Renal Insufficiency, Chronic/pathology ; Signal Transduction ; Transforming Growth Factor beta1/metabolism ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	Transforming Growth Factor beta1 ; Tumor Suppressor Protein p53
Language	English
Publishing date	2022-08-09
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	1358415-7
ISSN	1420-9071 ; 1420-682X
ISSN (online)	1420-9071
ISSN	1420-682X
DOI	10.1007/s00018-022-04505-w
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Article ; Online: The Cytoskeletal Network Regulates Expression of the Profibrotic Genes PAI-1 and CTGF in Vascular Smooth Muscle Cells.

Samarakoon, Rohan / Higgins, Paul J

Advances in pharmacology (San Diego, Calif.)

2017 Volume 81, Page(s) 79–94

Abstract: Vascular smooth muscle cells (VSMCs) are subject to changing hemodynamic stimuli that alter cytoskeletal dynamics, cellular architecture, and structure-associated signal transduction. Tensional stress, force application, and structural perturbations are ... ...

Abstract	Vascular smooth muscle cells (VSMCs) are subject to changing hemodynamic stimuli that alter cytoskeletal dynamics, cellular architecture, and structure-associated signal transduction. Tensional stress, force application, and structural perturbations are sensed by VSMCs and impact the physiological as well as pathophysiological responses of the vasculature. Microtubule-targeting drugs provide useful tools to analyze cytoskeletal-associated signaling pathways and their linkages to pathological outcomes. Architecture-based controls on a subset of profibrotic genes commonly expressed in vascular disease are highlighted by their frequent induction in mechanically manipulated cells and with associated changes in cytoskeletal dynamics. VSMCs respond to biomechanical cues by activating several kinase cascades, leading to gene reprogramming. It is apparent that a significant fraction of the vast repertoire of signaling intermediates, moreover, are sequestered on the cytoskeletal framework in an "inactive state." Reorganization within these networks due to fluctuating mechanical forces could release these effectors from their cytoskeletal anchors, thus alleviating the "repressive state" resulting in downstream signaling. Indeed, recent findings indicate that microtubule disruption in VSMCs rapidly stimulates pp60
MeSH term(s)	Animals ; Connective Tissue Growth Factor/genetics ; Fibrosis ; Gene Expression Regulation ; Humans ; Muscle, Smooth, Vascular/pathology ; Myocytes, Smooth Muscle/metabolism ; Myocytes, Smooth Muscle/pathology ; Plasminogen Activator Inhibitor 1/genetics
Chemical Substances	Plasminogen Activator Inhibitor 1 ; Connective Tissue Growth Factor (139568-91-5)
Language	English
Publishing date	2017-10-31
Publishing country	United States
Document type	Journal Article ; Review
ISSN	1557-8925
ISSN (online)	1557-8925
DOI	10.1016/bs.apha.2017.08.006
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Article ; Online: Increased mitochondrial calcium uptake and concomitant mitochondrial activity by presenilin loss promotes mTORC1 signaling to drive neurodegeneration.

Ryan, Kerry C / Ashkavand, Zahra / Sarasija, Shaarika / Laboy, Jocelyn T / Samarakoon, Rohan / Norman, Kenneth R

Aging cell

2021 Volume 20, Issue 10, Page(s) e13472

Abstract: Metabolic dysfunction and protein aggregation are common characteristics that occur in age-related neurodegenerative disease. However, the mechanisms underlying these abnormalities remain poorly understood. We have found that mutations in the gene ... ...

Abstract	Metabolic dysfunction and protein aggregation are common characteristics that occur in age-related neurodegenerative disease. However, the mechanisms underlying these abnormalities remain poorly understood. We have found that mutations in the gene encoding presenilin in Caenorhabditis elegans, sel-12, results in elevated mitochondrial activity that drives oxidative stress and neuronal dysfunction. Mutations in the human presenilin genes are the primary cause of familial Alzheimer's disease. Here, we demonstrate that loss of SEL-12/presenilin results in the hyperactivation of the mTORC1 pathway. This hyperactivation is caused by elevated mitochondrial calcium influx and, likely, the associated increase in mitochondrial activity. Reducing mTORC1 activity improves proteostasis defects and neurodegenerative phenotypes associated with loss of SEL-12 function. Consistent with high mTORC1 activity, we find that SEL-12 loss reduces autophagosome formation, and this reduction is prevented by limiting mitochondrial calcium uptake. Moreover, the improvements of proteostasis and neuronal defects in sel-12 mutants due to mTORC1 inhibition require the induction of autophagy. These results indicate that mTORC1 hyperactivation exacerbates the defects in proteostasis and neuronal function in sel-12 mutants and demonstrate a critical role of presenilin in promoting neuronal health.
MeSH term(s)	Alzheimer Disease/genetics ; Animals ; Caenorhabditis elegans/genetics ; Caenorhabditis elegans Proteins/metabolism ; Calcium/metabolism ; Mechanistic Target of Rapamycin Complex 1/metabolism ; Mitochondria/metabolism ; Neurodegenerative Diseases/genetics ; Neurodegenerative Diseases/pathology ; Presenilins/metabolism ; Signal Transduction
Chemical Substances	Caenorhabditis elegans Proteins ; Presenilins ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2021-09-09
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2113083-8
ISSN	1474-9726 ; 1474-9718
ISSN (online)	1474-9726
ISSN	1474-9718
DOI	10.1111/acel.13472
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Article: Emerging role of tumor suppressor p53 in acute and chronic kidney diseases

Overstreet, Jessica M. / Gifford, Cody C. / Tang, Jiaqi / Higgins, Paul J. / Samarakoon, Rohan

Cellular and molecular life sciences. 2022 Sept., v. 79, no. 9

2022

Abstract	p53 is a major regulator of cell cycle arrest, apoptosis, and senescence. While involvement of p53 in tumorigenesis is well established, recent studies implicate p53 in the initiation and progression of several renal diseases, which is the focus of this review. Ischemic-, aristolochic acid (AA) -, diabetic-, HIV-associated-, obstructive- and podocyte-induced nephropathies are accompanied by activation and/or elevated expression of p53. Studies utilizing chemical or renal-specific inhibition of p53 in mice confirm the pathogenic role of this transcription factor in acute kidney injury and chronic kidney disease. TGF-β1, NOX, ATM/ATR kinases, Cyclin G, HIPK, MDM2 and certain micro-RNAs are important determinants of renal p53 function in response to trauma. AA, cisplatin or TGF-β1–mediated ROS generation via NOXs promotes p53 phosphorylation and subsequent tubular dysfunction. p53-SMAD3 transcriptional cooperation downstream of TGF-β1 orchestrates induction of fibrotic factors, extracellular matrix accumulation and pathogenic renal cell communication. TGF-β1-induced micro-RNAs (such as mir-192) could facilitate p53 activation, leading to renal hypertrophy and matrix expansion in response to diabetic insults while AA-mediated mir-192 induction regulates p53 dependent epithelial G₂/M arrest. The widespread involvement of p53 in tubular maladaptive repair, interstitial fibrosis, and podocyte injury indicate that p53 clinical targeting may hold promise as a novel therapeutic strategy for halting progression of certain acute and chronic renal diseases, which affect hundreds of million people worldwide.
Keywords	acute kidney injury ; apoptosis ; aristolochic acids ; carcinogenesis ; cell communication ; cell cycle checkpoints ; cisplatin ; cyclins ; epithelium ; extracellular matrix ; fibrosis ; hypertrophy ; kidneys ; microRNA ; neoplasms ; phosphorylation ; phosphotransferases (kinases) ; therapeutics ; transcription (genetics) ; transcription factors
Language	English
Dates of publication	2022-09
Size	p. 474.
Publishing place	Springer International Publishing
Document type	Article
Note	Review
ZDB-ID	1358415-7
ISSN	1420-9071 ; 1420-682X
ISSN (online)	1420-9071
ISSN	1420-682X
DOI	10.1007/s00018-022-04505-w
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Article ; Online: The TGF-β1/p53/PAI-1 Signaling Axis in Vascular Senescence: Role of Caveolin-1.

Samarakoon, Rohan / Higgins, Stephen P / Higgins, Craig E / Higgins, Paul J

Biomolecules

2019 Volume 9, Issue 8

Abstract: Stress-induced premature cellular senescence is a significant factor in the onset of age-dependent disease in the cardiovascular system. Plasminogen activator inhibitor-1 (PAI-1), a major TGF-β1/p53 target gene and negative regulator of the plasmin-based ...

Abstract	Stress-induced premature cellular senescence is a significant factor in the onset of age-dependent disease in the cardiovascular system. Plasminogen activator inhibitor-1 (PAI-1), a major TGF-β1/p53 target gene and negative regulator of the plasmin-based pericellular proteolytic cascade, is elevated in arterial plaques, vessel fibrosis, arteriosclerosis, and thrombosis, correlating with increased tissue TGF-β1 levels. Additionally, PAI-1 is necessary and sufficient for the induction of p53-dependent replicative senescence. The mechanism of PAI-1 transcription in senescent cells appears to be dependent on caveolin-1 signaling.
MeSH term(s)	Animals ; Caveolin 1/metabolism ; Cellular Senescence ; Endothelium, Vascular/metabolism ; Humans ; Plasminogen Activator Inhibitor 1/metabolism ; Signal Transduction ; Transforming Growth Factor beta1/metabolism ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	Caveolin 1 ; Plasminogen Activator Inhibitor 1 ; Transforming Growth Factor beta1 ; Tumor Suppressor Protein p53
Language	English
Publishing date	2019-08-03
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2701262-1
ISSN	2218-273X ; 2218-273X
ISSN (online)	2218-273X
ISSN	2218-273X
DOI	10.3390/biom9080341
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