Involvement of PI3K, MAPK ERK1/2 and p38 in Functional Stimulation of Mesenchymal Progenitor Cells by Alkaloid Songorine

Zyuz’kov, G. N.; Zhdanov, V. V.; Мирошниченко, Л. А.; Удут, Е. В.; Chaikovskii, A. V.; Симанина, Е. В.; Данилец, М. Г.; Minakova, M. Yu.; Удут, В. В.; Толстикова, Т. Г.; Шульц, Э. Э.; Ставрова, Л. А.; Burmina, Ya. V.; Дыгай, А. М.

doi:10.1007/s10517-015-2889-6

Cited by 15 publications

(3 citation statements)

References 14 publications

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“…For example, SIRT3, an important member of the sirtuin family, can alleviate AKI by improving mitochondrial function and regulating fatty acid oxidation [ 17 , 24 ]. Mitogen-activated protein kinase 1 (MAPK1), also known as p38 or ERK, belongs to the MAP kinase family [ 25 , 26 ]. MAP kinases or ERKs were reported to function as an integration point for several biochemical signaling pathways and involve in various cellular processes like apoptosis, inflammation, and transcription regulation [ 27–30 ].…”

Section: Introductionmentioning

confidence: 99%

LncRNA KCNQ1OT1 (potassium voltage-gated channel subfamily Q member 1 opposite strand/antisense transcript 1) aggravates acute kidney injury by activating p38/NF-κB pathway via miR-212-3p/MAPK1 (mitogen-activated protein kinase 1) axis in sepsis

Wang

Mou

et al. 2021

Bioengineered

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Acute kidney injury (AKI), a common complication of sepsis, is characterized by a rapid loss of renal excretory function. A variety of etiologies and pathophysiological processes may contribute to AKI. Previously, mitogen-activated protein kinase 1 (MAPK1) was reported to regulate cellular processes in various sepsis-associated diseases. The current study aimed to further explore the biological function and regulatory mechanism of MAPK1 in sepsis-induced AKI. In our study, MAPK1 exhibited high expression in the serum of AKI patients. Functionally, knockdown of MAPK1 suppressed inflammatory response, cell apoptosis in response of lipopolysaccharide (LPS) induction in HK-2 cells. Moreover, MAPK1 deficiency alleviated renal inflammation, renal dysfunction, and renal injury in vivo . Mechanistically, MAPK1 could activate the downstream p38/NF-κB pathway. Moreover, long noncoding RNA potassium voltage-gated channel subfamily Q member 1 opposite strand/antisense transcript 1 (KCNQ1OT1) was identified to serve as a competing endogenous RNA for miR-212-3p to regulate MAPK1. Finally, rescue assays indicated that the inhibitory effect of KCNQ1OT1 knockdown on inflammatory response, cell apoptosis, and p38/NF-κB pathway was reversed by MAPK1 overexpression in HK-2 cells. In conclusion, KCNQ1OT1 aggravates acute kidney injury by activating p38/NF-κB pathway via miR-212-3p/MAPK1 axis in sepsis. Therefore, KCNQ1OT may serve as a potential biomarker for the prognosis and diagnosis of AKI patients.

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Section: Introductionmentioning

confidence: 99%

LncRNA KCNQ1OT1 (potassium voltage-gated channel subfamily Q member 1 opposite strand/antisense transcript 1) aggravates acute kidney injury by activating p38/NF-κB pathway via miR-212-3p/MAPK1 (mitogen-activated protein kinase 1) axis in sepsis

Wang

Mou

et al. 2021

Bioengineered

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“…Aconitum species have been reviewed broadly on the basis of their phytochemical constituents and uses . The main chemical constituents of Aconitum plants are alkaloids, flavonoids, saponins, saccharides and fatty acids.…”

Section: Introductionmentioning

confidence: 99%

“…1Aconitum species have been reviewed broadly on the basis of their phytochemical constituents and uses. [2][3][4][5][6] The main chemical constituents of Aconitum plants are alkaloids, flavonoids, saponins, saccharides and fatty acids. Aconitum alkaloids, which comprise C19-norditerpenoid alkaloids and C20-norditerpenoid alkaloids, are the dominant ingredients responsible for the pharmacological activity and therapeutic efficacy of Aconitum species.…”

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confidence: 99%

Aconitine induces cardiomyocyte damage by mitigating BNIP3‐dependent mitophagy and the TNFα‐NLRP3 signalling axis

Zhang

Wang

et al. 2019

Cell Proliferation

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Objectives Aconitine, the natural product extracted from Aconitum species, is widely used for the treatment of various diseases, including rheumatism, arthritis, bruises, fractures and pains. However, many studies have reported cardiotoxicity and neurotoxicity caused by aconitine, but the detailed mechanism underlying aconitine's effect on these processes remains unclear. Materials and methods The effects of aconitine on the inflammation, apoptosis and viability of H9c2 rat cardiomyocytes were evaluated by flow cytometry, Western blot, RNA sequencing and bioinformatics analysis. Results Aconitine suppressed cardiomyocyte proliferation and induced inflammation and apoptosis in a dose‐ and time‐dependent manner. These inflammatory damages could be reversed by a TNFα inhibitor and BNIP3‐mediated mitophagy. Consistent with the in vitro results, overexpression of BNIP3 in heart tissue partially suppressed the cardiotoxicity of aconitine by inhibiting apoptosis and the NLRP3 inflammasome. Conclusions Our findings lay a foundation for the application of a TNFα inhibitor and BNIP3 to aconitine‐induced cardiac toxicity prevention and therapy, thereby demonstrating potential for further investigation.

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Role of cAMP- and IKK-2-Dependent Signaling Pathways in Functional Stimulation of Mesenchymal Progenitor Cells with Alkaloid Songorine

et al. 2015

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The role of cAMP- and IKK-2-dependent pathways in stimulation of the growth capacity of mesenchymal progenitor cells with alkaloid songorine was studied in vitro. Inhibitors of adenylate cyclase and IKK-2 were shown to abolish the increase in proliferative activity of progenitor cells. Moreover, blockade of the inhibitory kinase complex was accompanied by a decrease in the intensity of progenitor cell differentiation.

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Involvement of PI3K, MAPK ERK1/2 and p38 in Functional Stimulation of Mesenchymal Progenitor Cells by Alkaloid Songorine

Cited by 15 publications

References 14 publications

LncRNA KCNQ1OT1 (potassium voltage-gated channel subfamily Q member 1 opposite strand/antisense transcript 1) aggravates acute kidney injury by activating p38/NF-κB pathway via miR-212-3p/MAPK1 (mitogen-activated protein kinase 1) axis in sepsis

LncRNA KCNQ1OT1 (potassium voltage-gated channel subfamily Q member 1 opposite strand/antisense transcript 1) aggravates acute kidney injury by activating p38/NF-κB pathway via miR-212-3p/MAPK1 (mitogen-activated protein kinase 1) axis in sepsis

Aconitine induces cardiomyocyte damage by mitigating BNIP3‐dependent mitophagy and the TNFα‐NLRP3 signalling axis

Role of cAMP- and IKK-2-Dependent Signaling Pathways in Functional Stimulation of Mesenchymal Progenitor Cells with Alkaloid Songorine

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