Relevance of Erk1/2-PI3K/Akt signaling pathway in CEES-induced oxidative stress regulates inflammation and apoptosis in keratinocytes

Sabnam, Silpa; Pal, Arttatrana

doi:10.1007/s10565-019-09467-7

Cited by 20 publications

(13 citation statements)

References 59 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The up-regulated expression levels of apoptosis and inflammation-related genes were also important indicators of tissue damages. A number of studies have demonstrated that cold stress causes the activation of extracellular signal-regulated kinases 1/2 (Erk1/2), major components of the greater mitogen-activated protein kinase (Mapk) cascade, which has been connected with increased inflammation and apoptosis ( Sabnam and Pal, 2019 ; Sun et al., 2020a , 2020b ). In this study, notable increases in Erk1/2 expression levels were found in elovl1a –/– and elovl1b –/– zebrafish under cold stress, compared with WT zebrafish ( Figure 3 F).…”

Section: Resultsmentioning

confidence: 99%

C24:0 avoids cold exposure-induced oxidative stress and fatty acid β-oxidation damage

2021

View full text Add to dashboard Cite

Section: Resultsmentioning

confidence: 99%

C24:0 avoids cold exposure-induced oxidative stress and fatty acid β-oxidation damage

2021

View full text Add to dashboard Cite

“…TCs increased epithelial cell sensitivity to LPS challenge as well as against PI3K p110δ and α/δ/β inhibitors, although the exact molecular mechanisms remain unclear. PI3K signaling pathway plays the important role in the regulation of cell responses to drugs (Sabnam and Pal, 2019 ). It seems that TCs can improve the capacity of epithelial cell bio-behaviors and functions during cell–cell interactions and the sensitivity of epithelia to pathogens or drugs in a non-specific pattern.…”

Section: Discussionmentioning

confidence: 99%

Roles of pulmonary telocytes in airway epithelia to benefit experimental acute lung injury through production of telocyte-driven mediators and exosomes

Tang

Song

et al. 2022

Cell Biol Toxicol

View full text Add to dashboard Cite

Background Telocytes (TCs) are experimentally evidenced as an alternative of cell therapies for organ tissue injury and repair. The aims of the present studies are to explore direct roles of TCs and the roles of TC-derived exosomes in support of experimental acute lung injury (ALI) in vivo or in vitro. Materials and methods The roles of TCs in experimental ALI were firstly estimated. Phosphoinositide 3-kinase (PI3K) p110δ and α/δ/β isoform inhibitors were used in study dynamic alterations of bio-behaviors, and in expression of functional factors of TCs per se and TC-co-cultured airway epithelial cells during the activation with lipopolysaccharide (LPS). TC-driven exosomes were furthermore characterized for intercellular communication by which activated or non-activated TCs interacted with epithelia. Results Our results showed that TCs mainly prevented from lung tissue edema and hemorrhage and decreased the levels of VEGF-A and MMP9 induced by LPS. Treatment with CAL101 (PI3K p110δ inhibitor) and LY294002 (PI3Kα/δ/β inhibitor) could inhibit TC movement and differentiation and increase the number of dead TCs. The expression of Mtor , Hif1α , Vegf-a , or Mmp9 mRNA increased in TCs challenged with LPS, while Mtor , Hif1α , and Vegf-a even more increased after adding CAL101 or Mtor after adding LY. The rate of epithelial cell proliferation was higher in co-culture of human bronchial epithelial (HBE) and TCs than that in HBE alone under conditions with or without LPS challenge or when cells were treated with LPS and CAL101 or LY294002. The levels of mTOR , HIF1α , or VEGF-A significantly increased in mono-cultured or co-cultured cells, challenged with LPS as compared with those with vehicle. LPS-pretreated TC-derived exosomes upregulated the expression of AKT, p-AKT, HIF1α, and VEGF-A protein of HBE. Conclusion The present study demonstrated that intraperitoneal administration of TCs ameliorated the severity of lung tissue edema accompanied by elevated expression of VEGF-A. TCs could nourish airway epithelial cells through nutrients produced from TCs, increasing epithelial cell proliferation, and differentiation as well as cell sensitivity to LPS challenge and PI3K p110δ and α/δ/β inhibitors, partially through exosomes released from TCs. Graphical abstract Supplementary Information The online version contains supplementary material available at 10.1007/s10565-021-09670-5.

show abstract

“…PI3K is an intracellular phosphatidylinositol kinase. When stimulated by stress signals, especially oxidative stress (Y. Zhang et al, 2021), PI3K is activated to produce the second messenger phosphatidylinositol 3,4,5‐trisphosphate (PIP3), and the PIP3 leads to the activation of AKT, which activates the downstream molecules Bcl‐2, Caspase 9, RIP1, MLKL, and so forth, and thus regulating cell proliferation, apoptosis, and necroptosis (Sabnam & Pal, 2019; J. Zhang et al, 2020). Particularly, BPA has shown apoptosis and necroptosis in chicken bursa through regulating oxidative stress and PI3K/AKT signaling pathway (L. Liu et al, 2021), and BPA caused apoptosis in pubertal SD rats testes and reproductive system via regulation of ROS/AKT/mTOR signaling pathway (Quan, Wang, Duan, Huang, Chen, et al, 2017; Quan, Wang, Duan, Huang, & Yang, 2017).…”

Section: Discussionmentioning

confidence: 99%

Bisphenol A aggravates renal apoptosis and necroptosis in selenium‐deficient chickens via oxidative stress and PI3K/AKT pathway

Chen

Zhang

Zou

et al. 2022

Journal Cellular Physiology

View full text Add to dashboard Cite

Bisphenol A (BPA) in the environment can have deleterious effects on humans and animals. BPA can exert nephrotoxicity by inducing oxidative stress. Selenium (Se) deficiency can specifically impair kidney tissues and additionally show a synergistic effect on the toxicity of several environmental chemicals. However, the toxic effects of BPA on the chicken kidney and whether Se deficiency produces synergistic effects on the toxicity of BPA remain poorly understood. Herein, we established BPA exposure models and Se deficiency model in vivo and in vitro, and described the discovery path of BPA aggravation on apoptosis and necroptosis in Se-deficient chicken kidneys via regulation of oxidative stress and phosphatidylinositol 3-kinase/ threonine kinase (PI3K/AKT) signaling pathway. We found that BPA exposure increased reactive oxygen species and malondialdehyde levels, reduced activities of catalase, GPx, and superoxide dismutase, downregulated PI3K and AKT expressions, activated Bcl/Bax-Caspase 9-Caspase 3, and receptor-interacting protein kinase 1/mixed lineage kinase domain-like protein signaling pathways, resulting in apoptosis and necroptosis in the chicken kidney. In addition, Se deficiency significantly promoted the expression of renal apoptosis and necroptosis in BPA-exposed chicken kidneys. Altogether, our results showed that BPA aggravates apoptosis and necroptosis in Sedeficient chicken kidneys via regulation of oxidative stress and PI3K/AKT signaling pathway. Our findings elucidate the mechanism of BPA nephrotoxicity and Se deficiency exacerbation toxicity in chickens and will provide great significance for the protection of the ecological environment and animal health.

show abstract

Relevance of Erk1/2-PI3K/Akt signaling pathway in CEES-induced oxidative stress regulates inflammation and apoptosis in keratinocytes

Cited by 20 publications

References 59 publications

C24:0 avoids cold exposure-induced oxidative stress and fatty acid β-oxidation damage

C24:0 avoids cold exposure-induced oxidative stress and fatty acid β-oxidation damage

Roles of pulmonary telocytes in airway epithelia to benefit experimental acute lung injury through production of telocyte-driven mediators and exosomes

Bisphenol A aggravates renal apoptosis and necroptosis in selenium‐deficient chickens via oxidative stress and PI3K/AKT pathway

Contact Info

Product

Resources

About