N-Acetylcysteine enhances the therapeutic efficacy of bone marrow-derived mesenchymal stem cell transplantation in rats with severe acute pancreatitis

Ma, Zhilong; Song, Guodong; Liu, Dalu; Qian, Daohai; Wang, Yuxiang; Zhou, Jia; Gong, Jian; Meng, Hui; Zhou, Bo; Yang, Tianshe; Zhang, Song

doi:10.1016/j.pan.2019.01.004

Cited by 19 publications

(15 citation statements)

References 35 publications

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“…Jung et al previously confirmed that human bone marrow-derived clonal MSCs could suppress inflammatory responses in rats with AP [16]. Our team has elucidated some of the important mechanisms by which MSCs attenuate SAP [17][18][19][20][21][22][23][24]. We found that MSCs can ameliorate SAP-associated multiple organ injury via suppression of autophagy [25], and we also detected statistically significant differences in the expression of long noncoding RNA H19 (LncRNA H19).…”

Section: Introductionsupporting

confidence: 60%

Long noncoding RNA H19 regulates the therapeutic efficacy of mesenchymal stem cells in rats with severe acute pancreatitis by sponging miR-138-5p and miR-141-3p

et al. 2020

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Background Patients with severe acute pancreatitis (SAP), which is characterized by high morbidity and mortality, account for an increasing medical burden worldwide. We previously found that mesenchymal stem cells (MSCs) could attenuate SAP and that expression of long noncoding RNA H19 (LncRNA H19) was upregulated in rats receiving MSCs. In the present study, we investigated the mechanisms of LncRNA H19 regulating the therapeutic efficacy of MSCs in the alleviation of SAP. Methods MSCs transfected with LncRNA H19 overexpression and knockdown plasmids were intravenously injected into rats 12 h after sodium taurocholate (NaT) administration to induce SAP. Results Overexpressing LncRNA H19 in MSCs significantly enhanced the anti-inflammatory capacity of the MSCs, inhibited autophagy via promotion of focal adhesion kinase (FAK)-associated pathways, and facilitated cell proliferation by increasing the level of β-catenin in rats with SAP. LncRNA H19 functioned as a competing endogenous RNA by sponging miR-138-5p and miR-141-3p. Knocking down miR-138-5p in MSCs increased the expression of protein tyrosine kinase 2 (PTK2, encoding FAK) to suppress autophagy, while downregulating miR-141-3p enhanced the level of β-catenin to promote cell proliferation. Conclusions In conclusion, LncRNA H19 effectively increased the therapeutic efficacy of MSCs in rats with SAP via the miR-138-5p/PTK2/FAK and miR-141-3p/β-catenin pathways.

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Section: Introductionsupporting

confidence: 60%

Long noncoding RNA H19 regulates the therapeutic efficacy of mesenchymal stem cells in rats with severe acute pancreatitis by sponging miR-138-5p and miR-141-3p

et al. 2020

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“…Hong previously con rmed that human bone marrow-derived clonal MSCs could suppress in ammatory responses in rats with AP [16]. Our team has elucidated some of the important mechanisms by which MSCs attenuate SAP [17][18][19][20][21][22][23][24]. We found that MSCs can ameliorate SAP-associated multiple-organ injury via suppression of autophagy [25], and we also detected statistically signi cant differences in the expression of long noncoding RNA H19 (LncRNA H19).…”

Section: Introductionmentioning

confidence: 70%

Long noncoding RNA H19 regulates the therapeutic efficacy of mesenchymal stem cells in rats with severe acute pancreatitis by sponging miR-138-5p and miR-141-3p

Song

Zhou

Song

et al. 2020

Preprint

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Background: Patients with severe acute pancreatitis (SAP), which is characterized by high morbidity and mortality, account for an increasing medical burden worldwide. We previously found that mesenchymal stem cells (MSCs) could attenuate SAP and that expression of long noncoding RNA H19 (LncRNA H19) was upregulated in rats receiving MSCs. In the present study, we investigated the mechanisms of LncRNA H19 regulating the therapeutic efficacy of MSCs in the alleviation of SAP.Methods: MSCs transfected with LncRNA H19 overexpression and knock down plasmids were intravenously injected into rats 12 h after sodium taurocholate (NaT) administration to induce SAP.Results: Overexpressing LncRNA H19 in MSCs significantly enhanced the anti-inflammatory capacity of the MSCs, inhibited autophagy via promotion of focal adhesion kinase (FAK)-associated pathways, and facilitated cell proliferation by increasing the level of β-catenin in rats with SAP. LncRNA H19 functioned as a competing endogenous RNA by sponging miR-138-5p and miR-141-3p. Knocking down miR-138-5p in MSCs increased the expression of protein tyrosine kinase 2 (PTK2, encoding FAK) to suppress autophagy, while downregulating miR-141-3p enhanced the level of β-catenin to promote cell proliferation.Conclusions: In conclusion, LncRNA H19 effectively increased the therapeutic efficacy of MSCs in rats with SAP via the miR-138-5p/PTK2/FAK and miR-141-3p/β-catenin pathways.

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“…The limited survival of engrafted MSCs and reduced resistance to oxidative and inflammatory stress at the injury site constrains its therapeutic efficacy. The treatment of MSCs with antioxidants found to ameliorate the therapeutic potential of MSCs in various disease models [57,58]. In contrast, it has been reported that high but non-toxic doses of antioxidants, when subjected to the proliferating MSCs, can cause DNA damage and induce premature senescence [59].…”

Section: Resultsmentioning

confidence: 99%

Insights into superoxide dismutase 3 in regulating biological and functional properties of mesenchymal stem cells

Sah

Agrahari

2020

Cell Biosci

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Mesenchymal stem cells (MSCs) have been extensively studied and implicated for the cell-based therapy in several diseases due to theirs immunomodulatory properties. Embryonic stem cells and induced-pluripotent stem cells have either ethical issues or concerns regarding the formation of teratomas, introduction of mutations into genome during prolonged culture, respectively which limit their uses in clinical settings. On the other hand, MSCs also encounter certain limitation of circumscribed survival and reduced immunomodulatory potential during transplantation. Plethora of research is undergoing to improve the efficacy of MSCs during therapy. Several compounds and novel techniques have been employed to increase the therapeutic potency of MSCs. MSCs secreted superoxide dismutase 3 (SOD3) may be the mechanism for exhibiting direct antioxidant activities by MSCs. SOD3 is a well known antioxidant enzyme and recently known to possess immunomodulatory properties. Along with superoxide scavenging property, SOD3 also displays anti-angiogenic, anti-chemotactic and anti-inflammatory functions in both enzymatic and nonenzymatic manners. In this review, we summarize the emerging role of SOD3 secreted from MSCs and SOD3's effects during cell-based therapy.

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N-Acetylcysteine enhances the therapeutic efficacy of bone marrow-derived mesenchymal stem cell transplantation in rats with severe acute pancreatitis

Cited by 19 publications

References 35 publications

Long noncoding RNA H19 regulates the therapeutic efficacy of mesenchymal stem cells in rats with severe acute pancreatitis by sponging miR-138-5p and miR-141-3p

Long noncoding RNA H19 regulates the therapeutic efficacy of mesenchymal stem cells in rats with severe acute pancreatitis by sponging miR-138-5p and miR-141-3p

Long noncoding RNA H19 regulates the therapeutic efficacy of mesenchymal stem cells in rats with severe acute pancreatitis by sponging miR-138-5p and miR-141-3p

Insights into superoxide dismutase 3 in regulating biological and functional properties of mesenchymal stem cells

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