A non-peptide probe for detecting chymotrypsin activity based on protection-deprotection strategy in living systems

2021 ◽  
Author(s):  
xiang Zou ◽  
Yuping Zhao ◽  
Chaofeng Lai ◽  
Yun Liang ◽  
Weiying Lin
Keyword(s):  
Cell Proliferation ◽  
Vital Role ◽  
Living Systems ◽  
Peptide Probe ◽  
Chymotrypsin Activity ◽  
Proliferation And Apoptosis ◽  
Abnormal Level

Chymotrypsin (CHT) plays a vital role in the metabolism of organisms, and affects the cell proliferation and apoptosis. Abnormal level of CHT will lead to a variety of diseases, such...

scholarly journals Modulation of Cathepsin S (CTSS) Regulates the Secretion of Progesterone and Estradiol, Proliferation, and Apoptosis of Ovarian Granulosa Cells in Rabbits

Animals ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 1770
Author(s):  
Guohua Song ◽  
Yixuan Jiang ◽  
Yaling Wang ◽  
Mingkun Song ◽  
Xuanmin Niu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Granulosa Cells ◽  
Hormone Secretion ◽  
Vital Role ◽  
Regulatory Function ◽  
Cathepsin S ◽  
Related Gene ◽  
Ovarian Granulosa Cells ◽  
Proliferation And Apoptosis

Cathepsin S (CTSS) is a member of cysteine protease family. Although many studies have demonstrated the vital role of CTSS in many physiological and pathological processes including tumor growth, angiogenesis and metastasis, the function of CTSS in the development of rabbit granulosa cells (GCS) remains unknown. To address this question, we isolated rabbit GCS and explored the regulatory function of the CTSS gene in cell proliferation and apoptosis. CTSS overexpression significantly promoted the secretion of progesterone (P4) and estrogen (E2) by increasing the expression of STAR and CYP19A1 (p < 0.05). We also found that overexpression of CTSS increased GCS proliferation by up-regulating the expression of proliferation related gene (PCNA) and anti-apoptotic gene (BCL2). Cell apoptosis was markedly decreased by CTSS activation (p < 0.05). In contrast, CTSS knockdown significantly decreased the secretion of P4 and E2 and the proliferation of rabbit GCS, while increasing the apoptosis of rabbit GCS. Taken together, our results highlight the important role of CTSS in regulating hormone secretion, cell proliferation, and apoptosis in rabbit GCS. These results might provide a basis for better understanding the molecular mechanism of rabbit reproduction.

scholarly journals The Expression Pattern of p32 in Sheep Muscle and Its Role in Differentiation, Cell Proliferation, and Apoptosis of Myoblasts

2019 ◽  
Vol 20 (20) ◽  
pp. 5161
Author(s):  
Jianyu Ma ◽  
Caifang Ren ◽  
Hua Yang ◽  
Jie Zhao ◽  
Feng Wang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Muscle Development ◽  
Developmental Stages ◽  
Vital Role ◽  
Myoblast Differentiation ◽  
Future Research ◽  
Fetal Sheep ◽  
Proliferation And Apoptosis ◽  
Sheep Muscle

The complement 1q binding protein C (C1QBP), also known as p32, is highly expressed in rapidly growing tissues and plays a crucial role in cell proliferation and apoptosis. However, there are no data interpreting its mechanisms in muscle development. To investigate the role of p32 in sheep muscle development, an 856 bp cDNA fragment of p32 containing an 837 bp coding sequence that encodes 278 amino acids was analyzed. We then revealed that the expression of p32 in the longissimus and quadricep muscles of fetal sheep was more significantly up-regulated than expression at other developmental stages. Furthermore, we found that the expression of p32 was increased during myoblasts differentiation in vitro. Additionally, the knockdown of p32 in sheep myoblasts effectively inhibited myoblast differentiation, proliferation, and promoted cell apoptosis in vitro. The interference of p32 also changed the energy metabolism from Oxidative Phosphorylation (OXPHOS) to glycolysis and activated AMP-activated protein kinase (AMPK) phosphorylation in sheep myoblasts in vitro. Taken together, our data suggest that p32 plays a vital role in the development of sheep muscle and provides a potential direction for future research on muscle development and some muscle diseases.

scholarly journals miR-22/TET2/p53-Feedback Loop Regulates Cell Proliferation and Apoptosis of k562 cells

2020 ◽  
Author(s):  
Hongxia Yao ◽  
Xiangjun Fu ◽  
Yueqing Chen ◽  
Mengling Duan ◽  
Li Guo ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Myeloid Leukemia ◽  
Feedback Loop ◽  
Feedback Regulation ◽  
K562 Cells ◽  
Vital Role ◽  
Luciferase Reporter ◽  
Luciferase Reporter Gene ◽  
Proliferation And Apoptosis

Abstract BackgroundChronic myeloid leukemia (CML) is a major global health threat due to its low cure rate and high fatality rate. Studies have reported that miR-22, TET2, and p53 play a vital role in the progression of leukemia. However, it is unclear whether there is feedback regulation between them.MethodsTransfection efficiency of miR-22 and TET2 was detected by qRT-PCR. CCK-8 assay was applied to measure the proliferation ability of K562 cells. Flow cytometry was used for evaluation the cell cycle and apoptosis rate of K562 cells after transfection. Moreover, the interaction between miR-22, TET2 and P53 was analyzed by luciferase reporter gene assay.ResultsExperiments indicated that the TET2 expression was decreased and apoptosis was increased in the miR-22 mimic group, and cell cycle was arrested in G0/G1phase, the proliferation was markedly inhibited. Meanwhile we found that TET2 can affect the expression of p53. Then, we directly proved p53 inhibition miR-22 transcription, whereas miR-22 as a transcriptional repressor, TET2 expression is negatively regulated to form a feedback loop.ConclusionsmiR-22, TET2 and p53 can form a feedback loop and thus affect cell proliferation and apoptosis of chronic myeloid leukemia cells.

scholarly journals Mir-573 regulates cell proliferation and apoptosis by targeting Bax in human degenerative disc cells following hyperbaric oxygen treatment

2020 ◽  
Author(s):  
Song-Shu Lin ◽  
Chi-Chien Niu ◽  
Li-Jen Yuan ◽  
Tsung-Ting Tsai ◽  
Po-Liang Lai ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Hyperbaric Oxygen ◽  
Caspase 3 ◽  
Target Genes ◽  
Vital Role ◽  
Luciferase Reporter ◽  
Nucleus Pulposus Cells ◽  
Caspase 9 ◽  
Proliferation And Apoptosis ◽  
Reporter Assays

Abstract Background: MicroRNA (miRNA) plays a vital role in the intervertebral disc (IVD) degeneration. The expression level of miR-573 was downregulated whereas Bax was upregulated notably in human degenerative nucleus pulposus cells (NPCs). In this study, we aimed to investigate the role of miR-573 in human degenerative NPCs following hyperbaric oxygen (HBO) treatment. Methods: NPCs were separated from human degenerated IVD tissues. The control cells were maintained in 5% CO2/95% air and the hyperoxic cells were exposed to 100% O2 at 2.5 atmospheres absolute. MiRNA expression profiling was performed via microarray and confirmed by real-time PCR, and miRNA target genes were identified using bioinformatics and luciferase reporter assays. The mRNA and protein levels of Bax were measured. The proliferation of NPCs were detected using MTT assay. The protein expression levels of Bax, cleaved caspase 9, cleaved caspase 3, pro-caspase 9 and pro-caspase 3 were examined.Results: Bioinformatics analysis indicated that the 3′ untranslated region (UTR) of the Bax mRNA contained the “seed-matched-sequence” for hsa-miR-573, which was validated via reporter assays. MiR-573 was induced by HBO and simultaneous suppression of Bax was observed in NPCs. Knockdown of miR-573 resulted in upregulation of Bax expression in HBO-treated cells. In addition, overexpression of miR-573 by HBO increased cell proliferation and coupled with inhibition of cell apoptosis. The cleavage of pro‑caspase 9 and pro‑caspase 3 was suppressed while the levels of cleaved caspase 9 and caspase 3 were decreased in HBO-treated cells. Transfection with anti-miR-573 partly suppressed the effects of HBO. Conclusion: Mir-573 regulates cell proliferation and apoptosis by targeting Bax in human degenerative NPCs following HBO treatment.

scholarly journals Androgen-Dependent Mechanisms of Wolffian Duct Development and Their Perturbation by Flutamide

Endocrinology ◽  
2006 ◽  
Vol 147 (10) ◽  
pp. 4820-4830 ◽  
Author(s):  
Michelle Welsh ◽  
Philippa T. K. Saunders ◽  
Nicholas I. Marchetti ◽  
Richard M. Sharpe
Keyword(s):  
Cell Proliferation ◽  
Androgen Receptor ◽  
Smooth Muscle Actin ◽  
Vital Role ◽  
Wolffian Duct ◽  
In Utero Exposure ◽  
Pregnant Rats ◽  
Androgen Receptor Antagonist ◽  
Proliferation And Apoptosis ◽  
Duct Development

Androgens play a vital role in Wolffian duct (WD) development, but the mechanisms that underlie this are unknown. The present study used in utero exposure of pregnant rats to the androgen receptor antagonist flutamide (50 or 100 mg/kg) to explore possible mechanisms. Pregnant rats were treated from embryonic d 15.5 (E15.5), and WDs were isolated from fetuses from E17.5–E21.5 and from adults. WD morphology was evaluated, and total length of the duct lumen was determined in fetal samples. Fetal WDs were immunostained for androgen receptor and stromal (inner and outer) and/or epithelial-cell-specific markers and analyzed for cell proliferation and apoptosis. In adulthood, most flutamide-exposed males lacked proximal WD-derived tissues, whereas at E18.5–E19.5, a time when the WD has completely regressed in females, a complete normal WD was present in all flutamide-exposed animals. This suggests that flutamide, at doses of 50 or 100 mg/kg, interferes with WD differentiation, not stabilization. Consistent with this, WD elongation/coiling increased in controls by 204% between E19.5 and E21.5 but increased less significantly (103%) in flutamide-exposed animals. This was associated with reduced cell proliferation, but there was no increase in apoptosis or change in expression of androgen receptor mRNA or protein. Flutamide treatment impaired differentiation of inner stromal cells, shown by decreased expression of smooth muscle actin, before effects were noted in the epithelium, consistent with androgens driving WD development via stromal-epithelial interactions. In conclusion, WD differentiation is far more susceptible to blockade of androgen action than is its initial stabilization, and these effects may be mediated by disruption of stromal-epithelial interactions.

Regional Association of Biological and Hemodynamic Parameters in Distal End-to-Side Vascular Anastomoses Perfused Ex Vivo

2002 ◽  
Author(s):  
Stephanie M. Kute ◽  
David A. Vorp
Keyword(s):  
Cell Proliferation ◽  
Graft Failure ◽  
Ex Vivo ◽  
Bypass Graft ◽  
Clinical Problem ◽  
Coagulation Factors ◽  
Vital Role ◽  
Vascular Bypass ◽  
Proliferation And Apoptosis ◽  
Biomechanical Forces

Vascular bypass graft failure is a significant clinical problem and is frequently due to the formation of intimal hyperplasia (IH) [1–3]. IH is characterized by the accumulation of smooth muscle cells (SMC) and extracellular matrix in the intima of the vessel, which occurs when the normal balance between vascular cell proliferation and apoptosis (regulated cell death) is altered [4]. The disturbed flow present at the anastomosis has been implicated in the formation of IH and the link between hemodynamics and graft failure is via a complex cascade of events whereby biomechanical forces cause biological responses [5, 6]. For example, immediate early genes (IEG) such as c-fos, c-jun and egr-1 are involved in the signaling pathways for proliferation and apoptosis. When extracellular biomechanical stimuli (e.g. shear stress) cause the expression of IEG, their protein products translocate to the nucleus. These proteins regulate the expression of a number of genes implicated in cardiovascular disease including growth factors, adhesion molecules, proapoptotic substrates and coagulation factors [7–9]. Because IEG are involved in both proliferation and apoptosis, their expression may upset the normal balance between cell proliferation and apoptosis and could play a vital role in the IH formation in vascular bypass grafts.

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