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Autophagy and KLOTHO

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https://www.readbyqxmd.com/read/27661766/decreased-level-of-klotho-contributes-to-drug-resistance-in-lung-cancer-cells-involving-in-klotho-mediated-cell-autophagy
#1
TianJun Chen, Hui Ren, Asmitanand Thakur, Tian Yang, Yang Li, Shuo Zhang, Ting Wang, MingWei Chen
Klotho is originally discovered as an anti-aging gene and recently identified as a tumor suppressor in various human cancers. Drug resistance is a major obstacle to affect the treatment of chemotherapy. In the present study, we explore the role of klotho on drug resistance in human lung cancers and investigate the mechanism of klotho on drug resistance in lung cancer cells. First, we detected a panel of six human lung cancer cell lines, including H460, SK-MES-1, cisplatin (DDP)-resistant A549/DDP, its parental subline A549, docetaxel (DTX)-resistant SPC-A-1/DTX, and SPC-A-1 by western blotting analysis...
September 23, 2016: DNA and Cell Biology
https://www.readbyqxmd.com/read/27125746/%C3%AE-klotho-and-chronic-kidney-disease
#2
J A Neyra, M C Hu
Alpha-Klotho (αKlotho) protein is encoded by the gene, Klotho, and functions as a coreceptor for endocrine fibroblast growth factor-23. The extracellular domain of αKlotho is cleaved by secretases and released into the circulation where it is called soluble αKlotho. Soluble αKlotho in the circulation starts to decline in chronic kidney disease (CKD) stage 2 and urinary αKlotho in even earlier CKD stage 1. Therefore soluble αKlotho is an early and sensitive marker of decline in kidney function. Preclinical data from numerous animal experiments support αKlotho deficiency as a pathogenic factor for CKD progression and extrarenal CKD complications including cardiac and vascular disease, hyperparathyroidism, and disturbed mineral metabolism...
2016: Vitamins and Hormones
https://www.readbyqxmd.com/read/26701976/%C3%AE-klotho-mitigates-progression-of-aki-to-ckd-through-activation-of-autophagy
#3
Mingjun Shi, Brianna Flores, Nancy Gillings, Ao Bian, Han Jun Cho, Shirley Yan, Yang Liu, Beth Levine, Orson W Moe, Ming Chang Hu
AKI confers increased risk of progression to CKD. αKlotho is a cytoprotective protein, the expression of which is reduced in AKI, but the relationship of αKlotho expression level to AKI progression to CKD has not been studied. We altered systemic αKlotho levels by genetic manipulation, phosphate loading, or aging and examined the effect on long-term outcome after AKI in two models: bilateral ischemia-reperfusion injury and unilateral nephrectomy plus contralateral ischemia-reperfusion injury. Despite apparent initial complete recovery of renal function, both types of AKI eventually progressed to CKD, with decreased creatinine clearance, hyperphosphatemia, and renal fibrosis...
August 2016: Journal of the American Society of Nephrology: JASN
https://www.readbyqxmd.com/read/26324504/haplodeficiency-of-klotho-gene-causes-arterial-stiffening-via-upregulation-of-scleraxis-expression-and-induction-of-autophagy
#4
Kai Chen, Xiaoli Zhou, Zhongjie Sun
The prevalence of arterial stiffness increases with age, whereas the level of the aging-suppressor protein klotho decreases with age. The objective of this study is to assess whether haplodeficiency of klotho gene causes arterial stiffness and to investigate the underlying mechanism. Pulse wave velocity, a direct measure of arterial stiffness, was increased significantly in klotho heterozygous (klotho(+/-)) mice versus their age-matched wild-type (WT) littermates, suggesting that haplodeficiency of klotho causes arterial stiffening...
November 2015: Hypertension
https://www.readbyqxmd.com/read/26061549/mammalian-target-of-rapamycin-signaling-inhibition-ameliorates-vascular-calcification-via-klotho-upregulation
#5
Yang Zhao, Ming-Ming Zhao, Yan Cai, Ming-Fei Zheng, Wei-Liang Sun, Song-Yang Zhang, Wei Kong, Jun Gu, Xian Wang, Ming-Jiang Xu
Vascular calcification (VC) is a major risk factor for cardiovascular mortality in chronic renal failure (CRF) patients, but the pathogenesis remains partially unknown and effective therapeutic targets should be urgently explored. Here we pursued the therapeutic role of rapamycin in CRF-related VC. Mammalian target of rapamycin (mTOR) signal was activated in the aortic wall of CRF rats. As expected, oral rapamycin administration significantly reduced VC by inhibiting mTOR in rats with CRF. Further in vitro results showed that activation of mTOR by both pharmacological agent and genetic method promoted, while inhibition of mTOR reduced, inorganic phosphate-induced vascular smooth muscle cell (VSMC) calcification and chondrogenic/osteogenic gene expression, which were independent of autophagy and apoptosis...
October 2015: Kidney International
https://www.readbyqxmd.com/read/25614163/mechanisms-of-development-of-multimorbidity-in-the-elderly
#6
REVIEW
Peter J Barnes
In ageing populations many patients have multiple diseases characterised by acceleration of the normal ageing process. Better understanding of the signalling pathways and cellular events involved in ageing shows that these are characteristic of many chronic degenerative diseases, such as chronic obstructive pulmonary disease (COPD), chronic cardiovascular and metabolic diseases, and neurodegeneration. Common mechanisms have now been identified in these diseases, which show evidence of cellular senescence with telomere shortening, activation of PI3K-AKT-mTOR signalling, impaired autophagy, mitochondrial dysfunction, stem cell exhaustion, epigenetic changes, abnormal microRNA profiles, immunosenescence and low grade chronic inflammation ("inflammaging")...
March 2015: European Respiratory Journal: Official Journal of the European Society for Clinical Respiratory Physiology
https://www.readbyqxmd.com/read/25377875/in-vivo-pancreatic-%C3%AE-cell-specific-expression-of-antiaging-gene-klotho-a-novel-approach-for-preserving-%C3%AE-cells-in-type-2-diabetes
#7
Yi Lin, Zhongjie Sun
Protein expression of an antiaging gene, Klotho, was depleted in pancreatic islets in patients with type 2 diabetes mellitus (T2DM) and in db/db mice, an animal model of T2DM. The objective of this study was to investigate whether in vivo expression of Klotho would preserve pancreatic β-cell function in db/db mice. We report for the first time that β-cell-specific expression of Klotho attenuated the development of diabetes in db/db mice. β-Cell-specific expression of Klotho decreased hyperglycemia and enhanced glucose tolerance...
April 2015: Diabetes
https://www.readbyqxmd.com/read/24347058/skeletal-muscle-mitochondrial-uncoupling-drives-endocrine-cross-talk-through-the-induction-of-fgf21-as-a-myokine
#8
Susanne Keipert, Mario Ost, Kornelia Johann, Francine Imber, Martin Jastroch, Evert M van Schothorst, Jaap Keijer, Susanne Klaus
UCP1-Tg mice with ectopic expression of uncoupling protein 1 (UCP1) in skeletal muscle (SM) are a model of improved substrate metabolism and increased longevity. Analysis of myokine expression showed an induction of fibroblast growth factor 21 (FGF21) in SM, resulting in approximately fivefold elevated circulating FGF21 in UCP1-Tg mice. Despite a reduced muscle mass, UCP1-Tg mice showed no evidence for a myopathy or muscle autophagy deficiency but an activation of integrated stress response (ISR; eIF2α/ATF4) in SM...
March 1, 2014: American Journal of Physiology. Endocrinology and Metabolism
https://www.readbyqxmd.com/read/23828695/klotho-acts-as-a-tumor-suppressor-in-cancers
#9
REVIEW
Biao Xie, Jinhui Chen, Bin Liu, Junkun Zhan
The klotho gene is a classical "aging suppressor" gene. Its roles in the pathology of chronic kidney diseases have been well documented. However, the role of Klotho in tumorigenesis, cancer progression, and prognosis is attracting more and more attention. Recent studies have shown that Klotho participates in the progression of several types of human cancers. Klotho functions as a tumor suppressor by inhibiting insulin/IGF1, p53/p21, and Wnt signaling. Silencing klotho gene expression is mainly mediated through promoter hypermethylation and histone deacetylation in cancer...
October 2013: Pathology Oncology Research: POR
https://www.readbyqxmd.com/read/23432957/restoration-of-klotho-gene-expression-induces-apoptosis-and-autophagy-in-gastric-cancer-cells-tumor-suppressive-role-of-klotho-in-gastric-cancer
#10
Biao Xie, Jianping Zhou, Guoshun Shu, Dong-Cai Liu, Jiapeng Zhou, Jinhui Chen, Lianwen Yuan
BACKGROUND: The loss of tumor suppressor gene expression is involved in the carcinogenesis of gastric cancer (GC). Klotho is a recently identified tumor suppressor gene that epigenetically inactivated in gastric cancer. However, the signaling pathways involved in the suppressive role of klotho have rarely been reported in gastric cancer. In this study, we investigated the involvement of klotho in gastric cancer cell proliferation, apoptosis, and autophagy as well as the associated signaling...
2013: Cancer Cell International
https://www.readbyqxmd.com/read/23248036/restoration-of-klotho-expression-induces-apoptosis-and-autophagy-in-hepatocellular-carcinoma-cells
#11
Guoshun Shu, Biao Xie, Feng Ren, Dong-cai Liu, Jiapeng Zhou, Qinglong Li, Jinhui Chen, Lianwen Yuan, Jianping Zhou
PURPOSE: Klotho has been identified as a tumor suppressor in several human malignancies including hepatocellular carcinoma (HCC). However, the signaling pathways involved in the tumor suppressive role of klotho in HCC have not been reported. Here, we investigated the role of klotho in HCC cell proliferation, apoptosis, autophagy, and invasion, as well as its associated signal transduction pathways. METHODS: Restoration of klotho gene expression was established by delivering a klotho gene expression vector into the human HCC cell lines HepG2 and MHCC-97-H...
April 2013: Cellular Oncology (Dordrecht)
https://www.readbyqxmd.com/read/21082218/autophagic-lysosomal-pathway-functions-in-the-masseter-and-tongue-muscles-in-the-klotho-mouse-a-mouse-model-for-aging
#12
Ryo-hei Iida, Syuhei Kanko, Takeo Suga, Mitsuhiko Morito, Akira Yamane
Klotho mutant (kl/kl) mice, a type of short-lived mouse models, display several aging-related phenotypes. To investigate whether the atrophy of skeletal muscles is induced in these mice via activation of the ubiquitin-proteasomal pathway and/or the autophagic-lysosomal pathway through an alteration of insulin/IGF-I signaling, we analyzed the activity of the two pathways for protein degradation and components of the insulin/IGF signaling pathway in their skeletal muscles. The masseter, tongue, and gastrocnemius muscles in kl/kl showed marked reductions in muscle weight and in myofiber diameter compared with +/+...
February 2011: Molecular and Cellular Biochemistry
https://www.readbyqxmd.com/read/19718893/-the-biology-of-aging
#13
Jean-Yves Le Gall, Raymond Ardaillou
Although aging is unavoidable, its course can be influenced by various factors, as illustrated by the increase in life expectancy associated with improvements in hygiene and with the general reduction in morbidity. Longevity has also been altered experimentally in some animal species. Aging follows a period of growth and reproduction. Death may occur when the immortality of the germinal line has been ensured. In other cases it results from gradual cellular deterioration. Four principal molecular and cellular processes have been studied in experimental models (mainly mice, worms and fruit flies):--inhibition of the insulin/IGF-1 axis increases life expectancy by allowing a transcription factor (DAF-16 in C...
February 2009: Bulletin de L'Académie Nationale de Médecine
https://www.readbyqxmd.com/read/18343589/morphological-and-biochemical-signs-of-age-related-neurodegenerative-changes-in-klotho-mutant-mice
#14
M Shiozaki, K Yoshimura, M Shibata, M Koike, N Matsuura, Y Uchiyama, T Gotow
Klotho mutant mice, defective in the klotho gene, develop multiple age-related disorders with very short lifespans. Introduction of the exogenous klotho gene into these mutant mice leads to an improvement in their phenotypes, while overexpression of this gene in wild-type mice significantly extends their lifespan. These observations suggest that the klotho gene/protein has an anti-aging function. Since there have been only a few reports with some disagreement about results on the CNS of the mutant mice, we tried to clarify whether the CNS neurons generate aging-like features, even in premature stages, using biochemical and morphological approaches...
April 9, 2008: Neuroscience
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