TAK1 mediates apoptosis via p38 involve in ischemia-induced renal fibrosis

Zhou, Jun; Zhong, Jiying; Huang, Zhenxing; Liao, Mengyang; Shi, Lin; Chen, Jia; Chen, Hongtao

doi:10.1080/21691401.2018.1442841

Cited by 18 publications

(11 citation statements)

References 37 publications

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“…Several research teams have reported that PTX-induced apoptosis is associated with p38 [8][9][10], JNK [7,8,12,13], ERK [8] and NF-jB [11], and TAK1 is a key kinase in these signal transduction pathways [15][16][17][18][20][21][22]. PTX mediated dose-and time-dependent induction of apoptosis and an increase in endogenous TAK1 and TAB1 levels.…”

Section: Tak1 Could Be Placed Between Ptx and Downstream Signalling Pmentioning

confidence: 99%

“…Many groups have proposed evidence for the role of TAK1 in the promotion of apoptosis: TAK1 mediates renal tubular epithelial cell apoptosis via the p38 signalling pathway [20], and TAK1 overexpression and Sef-S (similar expression to FGF genes, IL-17RD) enhance UV-induced HEK293T cell apoptosis [19]. In this work, PTX mediated dose-and time-dependent induction of endogenous TAK1 and TAB1 levels and, together with TAK1 overexpression, promoted HEK293 cells apoptosis more than PTX treated alone, suggesting that PTX induces apoptosis through the TAK1 activation pathway.…”

Section: With Ptx Treatment Tak1 Overexpression Promoted Hek293 Cellmentioning

confidence: 99%

“…TAB1 (TAK1-binding protein 1) is a TAK1binding protein [17,18]. TAK1 and TAB1 play an important role in cell apoptosis through the p38 [19,20], ERK [2], NF-jB [21,22] and JNK [19,23,24] signal transduction pathways.…”

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confidence: 99%

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Paclitaxel induces apoptosis through the TAK1–JNK activation pathway

Xiong

et al. 2020

FEBS Open Bio

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Paclitaxel (PTX) has previously been used to treat tumours of various tissue origins, such as lung, breast, ovarian, prostate cancers and leukemia. PTX-induced apoptosis is associated with p38 mitogen-activated protein kinase (p38 MAPK), extracellular signal-regulated kinase (ERK), nuclear factor-kappa B (NF-jB) and c-Jun N-terminal kinase or stress-activated protein kinase (JNK/ SAPK) pathways. Transforming growth factor-beta-activated kinase 1 (TAK1) and TAK1-binding protein 1 (TAB1) play an important role in cell apoptosis through the p38, ERK, NF-jB and JNK signal transduction pathways. To investigate the role of TAK1 in PTXinduced cell apoptosis, we treated HEK293 and 8305C cells with 0-20 µM PTX for 6, 12 or 24 h. To investigate whether TAK1 can cooperate with PTX for cancer treatment, we transfected cells with TAK1, TAB1 or control plasmid and treated them with PTX (3-10 µM) for 9-24 h. Apoptosis rates were analysed by flow cytometry (Annexin V/PI). Endogenous TAK1 and TAB1, caspase-7 cleavage, poly ADP-ribose polymerase (PARP) cleavage, Bcl-xL level, phospho-p44/42, phospho-JNK and phospho-p38 were detected by western blot. We show that in HEK293 and 8305C cells, PTX enhanced the endogenous TAK1/TAB1 level and induced cell apoptosis in a dose-and time-dependent manner. Upon TAK1 overexpression in HEK293 cells treated with PTX, apoptosis rate, JNK phosphorylation and PARP cleavage increased contrary to heat-shocked or untreated cells. CRISPR editing of the tak1 gene upon PTX treatment resulted in lower phospho-JNK and PARP cleavage levels than in cells transfected with the control or the TAK1-or TAB1 + TAK1-containing plasmids. TAK1-K63A could not induce JNK phosphorylation or PARP cleavage. We conclude that PTX induces HEK293 and 8305C cell apoptosis through the TAK1-JNK activation pathway, potentially highlighting TAK1's role in chemosensitivity.

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Section: Tak1 Could Be Placed Between Ptx and Downstream Signalling Pmentioning

confidence: 99%

Section: With Ptx Treatment Tak1 Overexpression Promoted Hek293 Cellmentioning

confidence: 99%

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Paclitaxel induces apoptosis through the TAK1–JNK activation pathway

Xiong

et al. 2020

FEBS Open Bio

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“…TAK1 is an important regulator of skeletal muscle fibre formation and plays important roles in cell division, proliferation, inflammation, and fibrosis. 8,9 The activation of TAK1 promotes fibrosis, 10,11 possibly because TAK1 activates the NF-κB pathway of muscular dystrophy fibroblasts. 9,11,12 TAK1 activation has been shown to promote the transformation of myoblasts into myofibroblasts.…”

Section: Introductionmentioning

confidence: 99%

A potential therapeutic effect of catalpol in Duchenne muscular dystrophy revealed by binding with TAK1

Zhao

Jiang

et al. 2020

J cachexia sarcopenia muscle

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Background Duchenne muscular dystrophy (DMD) is a progressive muscle disease caused by the loss of dystrophin, which results in inflammation, fibrosis, and the inhibition of myoblast differentiation in skeletal muscle. Catalpol, an iridoid glycoside, improves skeletal muscle function by enhancing myogenesis; it has potential to treat DMD. We demonstrate the positive effects of catalpol in dystrophic skeletal muscle. Methods mdx (loss of dystrophin) mice (n = 18 per group) were treated with catalpol (200 mg/kg) for six consecutive weeks. Serum analysis, skeletal muscle performance and histology, muscle contractile function, and gene and protein expression were performed. Molecular docking and ligand-target interactions, RNA interference, immunofluorescence, and plasmids transfection were utilized to explore the protective mechanism in DMD by which catalpol binding with transforming growth factor-βactivated kinase 1 (TAK1) in skeletal muscle. Results Six weeks of catalpol treatment improved whole-body muscle health in mdx mice, which was characterized by reduced plasma creatine kinase (n = 18, À35.1%, P < 0.05) and lactic dehydrogenase (n = 18, À10.3%, P < 0.05) activity. These effects were accompanied by enhanced grip strength (n = 18, +25.4%, P < 0.05) and reduced fibrosis (n = 18, À29.0% for hydroxyproline content, P < 0.05). Moreover, catalpol treatment protected against muscle fatigue and promoted muscle recovery in the tibialis anterior (TA) and diaphragm (DIA) muscles (n = 6, +69.8%, P < 0.05 and + 74.8%, P < 0.001, respectively), which was accompanied by enhanced differentiation in primary myoblasts from DMD patients (n = 6, male, mean age: 4.7 ± 1.9 years) and mdx mice. In addition, catalpol eliminated p-TAK1 overexpression in mdx mice (n = 12, À21.3%, P < 0.05) and primary myoblasts. The catalpol-induced reduction in fibrosis and increased myoblast differentiation resulted from the inhibition of TAK1 phosphorylation, leading to reduced myoblast trans-differentiation into myofibroblasts. Catalpol inhibited the phosphorylation of TAK1 by binding to TAK1, possibly at Asp-206, Thr-208, Asn-211, Glu-297, Lys-294, and Tyr-293. Conclusions Our findings show that catalpol and TAK1 inhibitors substantially improve whole-body muscle health and the function of dystrophic skeletal muscles and may provide a novel therapy for DMD.

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“…Previous studies confirmed that apoptosis was closely associated with renal fibrosis. Zhou Jun et al reported that TAK1 promoted renal fibrosis by regulating P38-induced apoptosis [10]. Xiangjun et al confirmed that puerarin could attenuate renal fibrosis by reducing epithelial cell apoptosis [11].…”

Section: Introductionmentioning

confidence: 99%

ShenShuai II Recipe Attenuates Apoptosis and Renal Fibrosis in Chronic Kidney Disease by Increasing Renal Blood Flow and Improving Oxygen Consumption

Wang

Yang

Zhou

et al. 2018

Evidence-Based Complementary and Alternative Medicine

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Background. Hypoxia plays a significant role in the progression of chronic kidney disease (CKD) and renal fibrosis. In China, Chinese herbal medicine has been widely used to treat CKD. ShenShuai II Recipe (SSR) is a commonly used prescription which has shown good results against CKD. However, the exact mechanisms of SSR are still unknown. In this study, chronic renal failure (CRF) was induced in rats by the 5/6 renal ablation/infarction (A/I) surgery; we investigated the efficacy and mechanisms of SSR on CKD in the current study. Male Sprague-Dawley (SD) rats were divided into the four groups: (1) sham operation group, (2) 5/6 (A/I) model group, (3) 5/6 (A/I) +SSR group, and (4) 5/6 (A/I) +Losartan group (5/6 (A/I) +Los). After 8 weeks of treatment, we evaluated renal blood flow (RBF) and oxygen consumption along with renal function, apoptosis, and renal fibrosis. Our results showed that SSR significantly improved RBF and reduced intrarenal oxygen consumption and apoptosis. Moreover, SSR markedly attenuated interstitial fibrosis, accompanied by decreased levels of serum creatinine (Scr), serum uric acid (UA), increased hemoglobin (HB), and evaluated glomerular filtration rates (eGFRs). These results suggest that SSR could mediate renal protection by improving intrarenal hypoxia and, furthermore, participate in the antiapoptotic effects by downregulating apoptosis markers (cleaved caspase-3 and the ratio of Bax/Bcl2) in 5/6 (A/I) model with CRF rats.

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TAK1 mediates apoptosis via p38 involve in ischemia-induced renal fibrosis

Cited by 18 publications

References 37 publications

Paclitaxel induces apoptosis through the TAK1–JNK activation pathway

Paclitaxel induces apoptosis through the TAK1–JNK activation pathway

A potential therapeutic effect of catalpol in Duchenne muscular dystrophy revealed by binding with TAK1

ShenShuai II Recipe Attenuates Apoptosis and Renal Fibrosis in Chronic Kidney Disease by Increasing Renal Blood Flow and Improving Oxygen Consumption

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