The sex determination and control of poultry is a key problem in production and scientific research despite few studies on regulatory factors, especially transcription factors in sex determination. In the early stage of this study, high-throughput sequencing was used to screen the differentially expressed gene JUN in male and female embryonic stem cells (ESCs) and primordial germ cells (PGCs). The qRT-PCR discovered that the JUN gene significantly increased from embryonic days (E) 2.5 later in chicken embryo development, and the female gonad expression was much higher than that of the male after E14.5. Lentivirus shRNA-JUN, shRNA-Smad2 interference, and OE-JUN overexpression vectors were successfully constructed. After interfering with JUN in vivo, male characteristics appeared in ZW embryonic gonads at E18.5. Meanwhile, the male-specific genes DMRT1 and Sox9 were upregulated, the female-specific genes FOXL2, ESR1, and CYP19A1 were downregulated, and the estradiol in the gonads was significantly decreased. The situation was reversed after the overexpression of JUN, ZZ chicken embryo developed into female sexual characteristics. The double luciferase report has found that the Smad2 promoter activity was significantly upregulated after interference with JUN, and significantly increased after the deletion of the JUN binding site. After the injection of the Smad2-shRNA vector into the blood vessel in vivo, it was discovered that DMRT1 and Sox9 of ZW embryos at E18.5 were downregulated, FOXL2 and CYP19A1 were significantly upregulated, and the gonads show femininity. In conclusion, this study proves that JUN is a key regulator in the process of chicken female sex differentiation, which can inhibit the transcription of Smad2 and promote the synthesis of estradiol, and participate in the process of chicken sex differentiation. This study lays a foundation for the analysis of the molecular mechanism of chicken sex determination and the development of poultry sex control technology.Our current research aimed to decipher the role and underlying mechanism with regard to miR-29b-3p involving in myocardial ischemia/reperfusion (I/R) injury. In the present study, cardiomyocyte H9c2 cell was used, and hypoxia/reoxygenation (H/R) model was established to mimic the myocardial I/R injury. The expressions of miR-29b-3p and pentraxin 3 (PTX3) were quantified deploying qRT-PCR and Western blot, respectively. The levels of LDH, TNF-α, IL-1β and IL-6 were detected to evaluate cardiomyocyte apoptosis and inflammatory response. Cardiomyocyte viability and apoptosis were examined employing CCK-8 assay and flow cytometry, respectively. Verification of the targeting relationship between miR-29b-3p and PTX3 was conducted using a dual-luciferase reporter gene assay. It was found that miR-29b-3p expression in H9c2 cells was up-regulated by H/R, and a remarkable down-regulation of PTX3 expression was demonstrated. MiR-29b-3p significantly promoted of release of inflammatory cytokines of H9c2 cells, and it also constrained the proliferation and promoted the apoptosis of H9c2 cells. Additionally, PTX3 was inhibited by miR-29b-3p at both mRNA and protein levels, and it was identified as a direct target of miR-29b-3p. PTX3 overexpression could reduce the inflammatory response, increase the viability of H9c2 cells, and inhibit apoptosis. Additionally, PTX3 counteracted the function of miR-29b-3p during the injury of H9c2 cells induced by H/R. In summary, miR-29b-3p was capable of aggravating the H/R injury of H9c2 cells by repressing the expression of PTX3.MicroRNA (miRNA) is an endogenous regulatory small molecule RNA. Growing evidence shows that miRNA plays an important regulatory role in gene expression. Although miRNA is a more intensive regulatory noncoding RNA in recent years, few studies have investigated the regulation of targeting genes involved in bone repair. Meanwhile, as a negative bone regulator, previous studies showed that casein kinase 2-interacting protein 1 (CKIP-1) is closely associated with bone formation and regeneration. https://www.selleckchem.com/products/gsk3787.html However, the gene knockout method may not be suitable for clinical application. Therefore, it was hypothesized that miRNA molecules can inhibit the expression of CKIP-1 and ultimately promote the osteogenesis process. The present study revealed that let-7i-5p plays an important role in the process of fracture healing by inhibiting the expression of CKIP-1. Related research provides a novel gene target for fracture healing. The online version of this article (10.1007/s10616-020-00444-1) contains supplementary material, which is available to authorized users. The online version of this article (10.1007/s10616-020-00444-1) contains supplementary material, which is available to authorized users.Secreted protein acidic and rich in cysteines-like 1 (SPARCL1) is implicated in tumor progression and considered as a tumor suppressor. Aim of the study is to investigate the role of SPARCL1 in the regulation of tumor biology. SPARCL1 expression in human cervical cells was determined through western blot and RT-PCR. The effects of SPARCL1 overexpression on cell proliferation, migration and invasion were evaluated through CCK8 assay, colony formation assay, Wound healing assay and Transwell assay, respectively. The gain function of Secreted phosphor protein 1 (SPP1) was also evaluated in these cell functions. We observed that SPARCL1 expression at protein levels and transcription levels was lower in HeLa cells than that in Ect1/E6E7 cells. When SPARCL1 was overexpressed in HeLa cells, cell proliferation, migration and invasion were greatly repressed. Additionally, SPARCL1 overexpression markedly downregulated SPP1 expression at transcription levels. Mechanistical study revealed that SPP1 overexpression could greatly counteract the effects of SPARCL1 overexpression on the aforementioned cell processes and inhibit the phosphorylation of focal adhesion kinase (FAK) and extracellular regulated protein kinases (ERK). Our findings indicated that HeLa cells overexpressing SPARCL1 showed weaker abilities of proliferation, migration and invasion, and its effects could be neutralized by SPP1 overexpression possibly via FAK/ERK pathway. The relationship of SPARCL1 and SPP1 could help us to further understand the pathogenesis of cervical cancer and SPARCL1/SPP1 could be beneficial therapeutic targets in cervical cancer.