scholarly journals Kochia scoparia Saponin Momordin Ic Modulates HaCaT Cell Proliferation and Apoptosis via the Wnt/β-Catenin Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Meijunzi Luo ◽  
Bijun Zeng ◽  
Haizhen Wang ◽  
Zhibo Yang ◽  
Youhua Peng ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Chinese Medicine ◽  
Hacat Cell ◽  
Alternative Therapy ◽  
Hacat Cells ◽  
Inhibitory Effects ◽  
Kochia Scoparia ◽  
Long Period ◽  
Pathway Activation ◽  
Proliferation And Apoptosis

Psoriasis is a chronic, recurrent, immunoinflammatory disease. For a long period, Traditional Chinese Medicine (TCM) is considered a reliable alternative therapy for patients with psoriasis. Fructus Kochiae (or Kochia scoparia) and its principle saponin, Momordin Ic, have been reported to protect against inflammation. Herein, we demonstrated that Momordin Ic could inhibit HaCaT cell proliferation and enhance cell apoptosis. In the meantime, Momordin Ic alters Wnt/β-catenin pathway activation by affecting β-catenin nuclear distribution. The Wnt/β-catenin signaling activator LiCl partially reversed the effects of Momordin Ic on HaCaT phenotypes and the Wnt/β-catenin pathway factors. Altogether, we demonstrate the inhibitory effects of Momordin Ic, one of the major saponin constituents of Fructus Kochiae, on HaCaT cell proliferation and Momordin Ic-induced alteration within the Wnt/β-catenin pathway. Momordin Ic might act on HaCaT cells by modulating the Wnt/β-catenin pathway.

MicroRNA-126-5p Regulates Proliferation and Apoptosis of IL-22-Stimulated Human Keratinocytes Through Regulating Caspase 1

2021 ◽  
Vol 11 (5) ◽  
pp. 1010-1016
Author(s):  
Weifeng Zha ◽  
Bo Guo ◽  
Shuyue Chen ◽  
Junwei Lu ◽  
Yunyun Shan
Keyword(s):  
Cell Proliferation ◽  
Protein Expression ◽  
Molecular Mechanisms ◽  
Cell Model ◽  
Luciferase Reporter ◽  
Control Group ◽  
Hacat Cells ◽  
Luciferase Reporter Gene ◽  
Proliferation And Apoptosis

Objective: The study was aimed to explore the roles of miR-126-5p in psoriasis and the underlying molecular mechanisms. Methods: In vitro cell model of psoriasis was established by IL-22 induction. CASP1, the target gene of miR-126-5p, was predicted by TargetScan and verified through the dual luciferase reporter gene system. qRT-PCR was used to measure the mRNA expression of miR-126-5p and CASP1 in IL-22 stimulated HaCaT cells. The protein expression of CASP1, cleaved-caspase3 and caspase3 were measured by Western blot analysis. MTT assay and flow cytometry analysis were performed to detect the cell proliferation and apoptosis. A Caspase3 Activity Assay kit was used to detect the activity of Caspase3. Results: miR-126-5p was high expressed in IL-22 stimulated HaCaT cells compared with normal HaCaT cells. We predicted and verified that CASP1 was a direct target of miR-126-5p, and the mRNA and protein expression of CASP1 were reduced in IL-22 stimulated HaCaT cells compared with the normal HaCaT cells. miR-126-5p inhibitor and CASP1-siRNA significantly decreased the expression of miR-126-5p and CASP1 in HaCaT cells respectively. miR-126-5p inhibitor up-regulated the expression of CASP1 in HaCaT cells, and the effect was reversed by the transfection with CASP1-siRNA. In comparison with the control group, miR-126-5p inhibitor decreased the cell proliferation, induced apoptosis, and improved the activity of Caspase3, enhanced cleaved-caspase3/caspase3 ratio in IL-22 stimulated HaCaT cells, and all the effects were reversed by down-regulating CASP1. Conclusion: We demonstrated that miR-126-5p inhibitor played a protective role in psoriasis by targeting CASP1, evidenced by inhibiting IL-22-induced HaCaT cell proliferation and inducing apoptosis.

miR-338-3p inhibits HIF-1α to Attenuate Nucleus Pulposus Cell Proliferation and Promote Apoptosis Through the Hippo-YAP Pathway

2021 ◽  
Author(s):  
Daolu Zhan ◽  
Jian Liu ◽  
Mingxia Lin ◽  
Jian Chen ◽  
Yehan Fang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Nucleus Pulposus ◽  
Intervertebral Disc Degeneration ◽  
Nucleus Pulposus Cell ◽  
Luciferase Assay ◽  
Ki 67 ◽  
Pathway Activation ◽  
Proliferation And Apoptosis ◽  
Related Proteins

Abstract The proliferation and apoptosis of nucleus pulposus (NP) cells (NPCs) play a crucial role in intervertebral disc degeneration (IDD). we aimed to discover the role of miRNA-induced IDD. We analyzed the miRNA expression of three NP tissues from IDD patients and three normal NP samples using the GEO2R tool, and The results revealed that miR-338-3p was upregulated in NPCs from IDD patients. miR-338-3p suppressed NPCs proliferation, and the related proteins PCNA and Ki-67 were downregulated, as demonstrated via western blotting. miR-338-3p promoted apoptosis. Furthermore, we predicted that HIF-1α was targeted by miR-338-3p, using the miRDB database, and this target was validated via dual luciferase assay. HIF-1α reversed miR-338-3p-induced NPCs proliferation and apoptosis. The Hippo-YAP pathway activation proteins YAP, CTGF, and PCNA were upregulated, unlike the inhibitory YAP phosphorylation. In conclusions, our results suggestive that miR-338-3p inhibited HIF-1α/ Hippo-YAP pathway to attenuate NPCs proliferation and apoptosis.

scholarly journals Tetrandrine inhibits the proliferation and cytokine production induced by IL-22 in HaCaT cells

2018 ◽  
Vol 46 (12) ◽  
pp. 5210-5218 ◽  
Author(s):  
Fang Wang ◽  
Jun Wang ◽  
Zhuo Zhang ◽  
Siwei Chen
Keyword(s):  
Cell Proliferation ◽  
Western Blot ◽  
Cytokine Production ◽  
Hacat Cell ◽  
Quantitative Polymerase Chain Reaction ◽  
Underlying Mechanism ◽  
Inhibitory Effect ◽  
Enzyme Linked Immunosorbent Assay ◽  
Hacat Cells ◽  
Stat3 Phosphorylation

Objective To investigate the effect of tetrandrine (Tet) on HaCaT cell proliferation and cytokine expression induced by interleukin (IL)-22, and to investigate the underlying mechanism. Methods The half maximal inhibitory concentration (IC50) and antiproliferation effects of Tet on IL-22-treated HaCaT cells were analysed by MTT assay. Signal transducer and activator of transcription 3 ( STAT3) expression was measured by reverse transcription plus real-time quantitative polymerase chain reaction (qPCR) and by Western blot. Phosphorylated (p)-STAT3 levels were also measured by Western blot. Cytokine production by HaCaT cells was analysed by enzyme-linked immunosorbent assay (ELISA) following administration of IL-22 and/or Tet. Results Tet displayed a dose-dependent inhibitory effect on HaCaT cell proliferation and reduced the phosphorylation level of STAT3 induced by IL-22, without affecting STAT3 mRNA and protein levels. Furthermore, co-incubation with Tet significantly down-regulated HaCaT cell production of tumour necrosis factor (TNF)-α, IL-1β, IL-6, IL-20 and chemokine (C-C motif) ligand 20 (CCL20) induced by IL-22. Conclusions Tet inhibits proliferation and cytokine production in HaCaT cells, and the process may involve the inhibition of STAT3 phosphorylation.

scholarly journals Possible treatment for cutaneous lichen planus: An in vitro anti-inflammatory role of Angelica polysaccharide in human keratinocytes HaCaT

2019 ◽  
Vol 33 ◽  
pp. 205873841882183 ◽  
Author(s):  
Jun Wang ◽  
Guanzhi Chen ◽  
Tongxin Shi ◽  
Yingying Wang ◽  
Chengfei Guan
Keyword(s):  
Cell Viability ◽  
Lichen Planus ◽  
Inflammatory Cytokines ◽  
Cell Injury ◽  
Hacat Cell ◽  
Human Keratinocytes ◽  
Hacat Cells ◽  
Protective Effects ◽  
Inhibitory Effects ◽  
Inflammatory Injury

Cutaneous lichen planus (CLP) is an autoimmune disease. Angelica polysaccharide (AP) has been found to exert immunomodulation activity. In this study, we explored the roles of AP in lipopolysaccharide (LPS)-induced inflammatory injury of human keratinocytes (HaCaT cells), as well as the underlying mechanisms. LPS-induced cell injury was evaluated by alterations of cell viability, apoptosis, and expressions of proteins associated with apoptosis and inflammatory cytokines. Then, the protective effects of AP on LPS-induced cell injury were assessed. The protein expressions of sirtuin 1 (SIRT1) and key kinases in the Nrf2/HO-1 and nuclear factor κB (NF-κB) pathways were measured using western blotting. SIRT1 knockdown and overexpression were used to analyze whether AP affected HaCaT cells through regulating SIRT1. Finally, the possible inhibitory effects of AP on cell injury after LPS treatment were also evaluated. We found that LPS reduced HaCaT cell viability, enhanced apoptosis, and induced release of inflammatory cytokines. AP alleviated LPS-induced HaCaT cell inflammatory injury. The expression of SIRT1 was enhanced after AP treatment. AP activated Nrf2/HO-1 pathway while inhibited NF-κB pathway in HaCaT cells. The protective effects of AP on LPS-induced HaCaT cell injury were reversed by SIRT1 knockdown. Dysregulation of SIRT1 altered the activation of Nrf2/HO-1 and NF-κB pathways in LPS-treated HaCaT cells. Furthermore, AP also exerted inhibitory effects on HaCaT cell injury after LPS stimulation. In conclusion, AP could alleviate LPS-induced inflammatory injury of HaCaT cells through upregulating SIRT1 expression and then activating Nrf2/HO-1 pathway but inactivating NF-κB pathway. This study provided a possible therapeutic strategy for clinical CLP treatments.

scholarly journals Mechanistic effect of the human GJB6 gene and its mutations in HaCaT cell proliferation and apoptosis

2018 ◽  
Vol 51 (9) ◽  
Author(s):  
Yuting Lu ◽  
Ruili Zhang ◽  
Zhenying Wang ◽  
Shuhua Zhou ◽  
Yali Song ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Hacat Cell ◽  
Proliferation And Apoptosis

Dermal Mesenchymal Stem Cells from Psoriatic Lesions Stimulate HaCaT Cell Proliferation, Differentiation, and Migration via Activating the PI3K/AKT Signaling Pathway

Dermatology ◽  
2021 ◽  
pp. 1-9
Author(s):  
Nannan Liang ◽  
Wenjuan Chang ◽  
Aihong Peng ◽  
Yue Cao ◽  
Junqin Li ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cell Proliferation ◽  
Signaling Pathway ◽  
Hacat Cell ◽  
Akt Signaling ◽  
Hacat Cells ◽  
Akt Signaling Pathway ◽  
Expression Levels ◽  
Proliferation And Differentiation ◽  
And Migration

<b><i>Background:</i></b> Psoriasis is a chronic inflammatory skin disease characterized by excessive proliferation and abnormal differentiation of keratinocytes. Dermal mesenchymal stem cells (DMSCs) are not only involved in the regeneration of skin tissue, but also can regulate skin microenvironment by secreting cytokines. However, whether and how psoriatic DMSCs regulate proliferation and differentiation of keratinocytes remains unknown. <b><i>Objective:</i></b> To study the effects of psoriatic DMSCs on the proliferation, differentiation, and migration of keratinocytes and the underlying mechanisms. <b><i>Methods:</i></b> Following co-cultures of HaCaT cells with either psoriatic DMSCs (p-DMSCs) or DMSCs from normal volunteers (n-DMSCs), HaCaT cell proliferation was assessed using CCK-8 and EDU incorporation assay, while scratch assay and transwell assay were used to assess cell migration. qRT-PCR was used to determine expression levels of mRNA for cell proliferation (Ki-67) and differentiation (keratin 5, involucrin, and filaggrin). Western blot was used to measure expression levels of proteins associated with keratinocyte proliferation and differentiation in cultured HaCaT cells treated with or without PI3K inhibitor. ELISA assay was used to measure expression profile of stem cell factor (SCF), epidermal growth factor (EGF), and interleukin-11 (IL-11) within the co-culture supernatants. <b><i>Results:</i></b> The results showed that p-DMSCs displayed a higher potency than n-DMSCs in stimulating proliferation, differentiation, and migration of HaCaT cells. Expression levels of PI3K and AKT proteins were markedly increased in HaCaT cells co-cultured with DMSCs versus HaCaT cell culture alone. Moreover, inhibition of the PI3K/AKT signaling pathway reversed the effect of p-DMSCs on proliferation, differentiation, and migration of HaCaT cells. Compared with n-DMSCs, the p-DMSCs showed increased secretion of IL-11, EGF, and SCF. <b><i>Conclusion:</i></b> p-DMSCs stimulate HaCaT cell proliferation, differentiation and migration via activating the PI3K/AKT signaling pathway, providing a new insight into the pathogenesis of psoriasis.

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