Retracted: Baicalein retards proliferation and collagen deposition by activating p38MAPK‐JNK via microRNA‐29

Abstract

Immoderate proliferation and deposition of collagen generally result in hypertrophic scars and even keloids. microRNA‐29 (miR‐29) has been proved as a crucial regulator in these pathological processes. Although mounting evidence have proved baicalein (BAI) impairs scar formation, it is still incompletely understood whether miR‐29 participated in the underlying mechanism. In the present study, NIH‐3T3 cells were stimulated with BAI, and then cell viability was analyzed by cell counting kit‐8 (CCK‐8) and Western blot. We further analyzed total soluble collagen, collagen 1, and alpha‐smooth muscle actin (α‐SMA) in NIH‐3T3 cells, which were exposed to transforming growth factor beta 1 (TGF‐β1)/BAI, using a Sircol assay kit, quantitative reverse transcription‐PCR (qRT‐PCR) and Western blot, respectively. Besides, the miR‐29 inhibitor was transduced and its transfection efficiency was verified by qRT‐PCR. Finally, the phosphorylated p38 mitogen‐activated protein kinase (p38MAPK) and c‐Jun N‐terminal kinase (JNK) were examined by Western blot. BAI effectively retarded NIH‐3T3 proliferation in a dose‐dependent manner. Besides, TGF‐β1‐induced deposition of total soluble collagen and synthesis of collagen 1 and α‐SMA were repressed by BAI at mRNA and protein levels. However, miR‐29 inhibitor reversed the effects of BAI. Remarkably, BAI promoted phosphorylated expression of p38MAPK and JNK while miR‐29 inhibitor reversed its effects on the phosphorylated expression of p38MAPK and JNK. BAI effectively weakened the cell viability and repressed TGF‐β1‐induced total soluble collagen as well as collagen 1 and α‐SMA by upregulating miR‐29. Mechanically, BAI activates the p38MAPK/JNK pathway by promoting miR‐29.

Baicalein Induces Apoptosis of Pancreatic Cancer Cells by Regulating the Expression of miR-139-3p and miR-196b-5p

“…Baicalein decreased the expression level of miR-424-3p in lung cancer to suppress cell proliferation and improve cisplatin sensitivity (13). Baicalein activates p38-MAPK-JNK pathway via increasing the expression level of miR-29 to retard proliferation and collagen deposition (30). To date, few studies reported whether baicalein could alter several specific miRNAs expression pattern to further affect the progression of pancreatic cancer.…”

Baicalein Alleviates Fibrosis and Inflammation in Scleroderma Through Regulating B Cell Abnormalities

“…Many researches have reported that baicalein exerted certain therapeutic effects on pulmonary brosis, hepatic brosis, cardiac brosis and renal interstitial brosis [8][9][10][11]. 150 µM baicalein suppressed TGF-β1induced collagen deposition as well as the expression of collagen I and α-SMA by activating p38MAPK/JNK pathway in NIH-3T3 cells [14]. Baicalein was also found to attenuate the production of type I collagen, downregulate expression of CTGF and α-SMA and retard α-SMA lament formation in TGF-β1-stimulated human lung broblasts [8,13].…”

“…Previous studies have reported that it has been increasingly used against pulmonary, hepatic, cardiac and renal brosis as potential therapeutic agents [8][9][10][11]. The suppression of brosis by baicalein was partially attributed to the attenuation of collagen and ECM production [12][13][14][15], inhibition of cell proliferation and induction of apoptosis of broblasts [16], inhibition of myo brolast differentiation [8] and downregulation of brogenic markers expression [9,13,14].Collectively, baicalein modulates pro-brotic and in ammatory pathways, then results in the inhibition of brosis in different organs. However, the effect of baicalein against SSc and the exact molecular mechanisms responsible for its effect have not been elucidated.…”

Role of Wnt5a in periodontal tissue development, maintenance, and periodontitis: Implications for periodontal regeneration (Review)

“…Wnt5a inhibited the induction of DFCs cellular senescence, supported cell proliferation and prevented cell death (59). Wnt5a significantly enhanced the proliferation of HPDLCs by phosphorylating two major mitogen-activated protein kinases, extracellular signal-regulated kinase and Jnk (27), which are important signaling molecules influencing cell proliferation (60). In addition, Wnt5a promoted the migration of HPDLCs by phosphorylating Akt, which serves pivotal roles in cell migration (61).…”