miRNA-489-3p Improves Sepsis-Induced Lung Injury by Regulating Toll-Like Receptor 4 (TLR4) Signaling Pathway

Aim: To discuss miRNA-489-3p in sepsis-induced lung injury. Materials and methods: Using NR-8383 as research cell in our study, and using LPS stimulation to sepsis induced lung injury vitro model. Measuring cell proliferation by MTS assay; using Elisa assay to measure IL-1β, IL-6 and TNF-α concentration; apoptosis cell number and apoptosis rate were evaluated using TUNEL and flow cytometry; gene and protein were measured by RT-PCR and WB assay; measuring p-NF-κB(p65) nuclear volume by Immunofluorescence (IF); using Luciferase reporter assay to analysis miRNA-489-3p and TLR4 correlation. Results: Cell proliferation rate significantly down-regulated (P < 0.001), apoptosis cell number and apoptosis rate significantly increased (P < 0.001); IL-1β, IL-6 and TNF-α concentrations significantly up-regulated (P < 0.001); TLR4 and MyD88 gene and protein significantly increased (P < 0.001), NF-κB(p65) mRNA and p-NF-κB(p65) protein and nuclear volume significantly increased (P < 0.001). However, with miRNA-489-3p supplement, the cell proliferation rate, apoptosis cell number and apoptosis rate were significantly improved (P < 0.001, respectively) via TLR4, MyD88 and NF-κB(p65) mRNA and protein significantly depressing (P < 0.001, respectively). By LUC assay, miRNA-489-3p could target to TLR4 in NR-8383 cell. Conclusion: miRNA-489-3p overexpression had effect to improve sepsis induced lung injury via regulation TLR4/MyD88/NF-κB(p65).

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Evidence for a Negative Correlation between Human Reactive Enamine-Imine Intermediate Deaminase A (RIDA) Activity and Cell Proliferation Rate: Role of Lysine Succinylation of RIDA

International Journal of Molecular Sciences ◽

10.3390/ijms22083804 ◽

2021 ◽

Vol 22 (8) ◽

pp. 3804

Author(s):

Luisa Siculella ◽

Laura Giannotti ◽

Benedetta Di Chiara Stanca ◽

Matteo Calcagnile ◽

Alessio Rochira ◽

...

Keyword(s):

Cell Proliferation ◽

Cell Lines ◽

Negative Correlation ◽

Cancer Biology ◽

Human Tumor ◽

In Silico Analysis ◽

Proliferation Rate ◽

Reactive Intermediate ◽

Cell Proliferation Rate

Reactive intermediate deaminase (Rid) proteins are enzymes conserved in all domains of life. UK114, a mammalian member of RidA subfamily, has been firstly identified as a component of liver perchloric acid-soluble proteins (L-PSP). Although still poorly defined, several functions have been attributed to the mammalian protein UK114/RIDA, including the reactive intermediate deamination activity. The expression of UK114/RIDA has been observed in some tumors, arousing interest in this protein as an evaluable tumor marker. However, other studies reported a negative correlation between UK114/RIDA expression, tumor differentiation degree and cell proliferation. This work addressed the question of UK114/RIDA expression in human non-tumor HEK293 cell lines and in some human tumor cell lines. Here we reported that human RIDA (hRIDA) was expressed in all the analyzed cell line and subjected to lysine (K-)succinylation. In HEK293, hRIDA K-succinylation was negatively correlated to the cell proliferation rate and was under the control of SIRT5. Moreover, K-succinylation clearly altered hRIDA quantification by immunoblotting, explaining, at least in part, some discrepancies about RIDA expression reported in previous studies. We found that hRIDA was able to deaminate reactive enamine-imine intermediates and that K-succinylation drastically reduced deaminase activity. As predicted by in silico analysis, the observed reduction of deaminase activity has been related to the drastic alterations of hRIDA structure inferred by K-succinylation. The role of hRIDA and the importance of its K-succinylation in cell metabolism, especially in cancer biology, have been discussed.

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Cell proliferation rate and nuclear morphometry in Roberts syndrome

Clinical Genetics ◽

10.1111/j.1399-0004.1998.tb03772.x ◽

2008 ◽

Vol 54 (6) ◽

pp. 512-516 ◽

Cited By ~ 6

Author(s):

Petros M Pavlopoulos ◽

Anastasia E Konstantinidou ◽

Emmanuel Agapitos ◽

Panagiotis Davaris

Keyword(s):

Cell Proliferation ◽

Proliferation Rate ◽

Roberts Syndrome ◽

Nuclear Morphometry ◽

Cell Proliferation Rate

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Analysis of cell proliferation rate in Oral Leukoplakia and Oral Squamous Cell Carcinoma

Journal of Clinical and Experimental Dentistry ◽

10.4317/jced.2.e173 ◽

2010 ◽

pp. e173-177 ◽

Cited By ~ 2

Author(s):

S. Mehkri ◽

AR. Iyengar ◽

KS. Nagesh ◽

MB. Bharati

Keyword(s):

Cell Proliferation ◽

Squamous Cell Carcinoma ◽

Oral Squamous Cell Carcinoma ◽

Cell Carcinoma ◽

Squamous Cell ◽

Proliferation Rate ◽

Oral Leukoplakia ◽

Cell Proliferation Rate

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Parathyroid gland volume increases with postmaturational aging in the rat

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00261.2001 ◽

2002 ◽

Vol 282 (3) ◽

pp. E557-E563 ◽

Cited By ~ 7

Author(s):

Bernard Halloran ◽

Per Udén ◽

Quan-Yang Duh ◽

Shoichi Kikuchi ◽

Tracy Wieder ◽

...

Keyword(s):

Cell Proliferation ◽

Renal Insufficiency ◽

Parathyroid Gland ◽

Inorganic Phosphorus ◽

Proliferation Rate ◽

Parathyroid Cell ◽

Fischer 344 ◽

Gland Volume ◽

Cell Proliferation Rate ◽

Age Related

To examine the pathophysiology of the age-related rise in the plasma concentration of parathyroid hormone (PTH), we studied the relationships among plasma immunoreactive PTH (iPTH), parathyroid gland volume, parathyroid cell proliferation rate, renal function, and blood Ca2+ in male Fischer 344 rats aged 6–28 mo. Plasma iPTH increased 2.5-fold between 6 and 28 mo and correlated with parathyroid gland volume ( r = 0.87). Gland volume began to increase as early as 6–12 mo of age and by 28 mo was threefold greater than at 6 mo. Gland expansion was a consequence of hyperplasia stimulated in part by an increase in cell proliferative activity late in life. Blood Ca2+ and plasma inorganic phosphorus did not change significantly with age. Glomerular filtration rate decreased with age but only after the age of 24 mo. Unlike what has been observed in the human, these data suggest that the age-related increase in plasma iPTH in the rat is linked to parathyroid gland hyperplasia and that early gland growth does not appear to be associated with hypocalcemia or renal insufficiency, but rather to developmentally related metabolic changes. Later in life (>24 mo), the increase in parathyroid cell proliferation rate, further hyperplastic expansion of the gland, and increase in iPTH secretion appear to be associated with renal insufficiency.

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The Novel Long Noncoding RNA TUSC7 Inhibits Proliferation by Sponging MiR-211 in Colorectal Cancer

Cellular Physiology and Biochemistry ◽

10.1159/000457938 ◽

2017 ◽

Vol 41 (2) ◽

pp. 635-644 ◽

Cited By ~ 57

Author(s):

Jian Xu ◽

Rui Zhang ◽

Jian Zhao

Keyword(s):

Colorectal Cancer ◽

Cell Proliferation ◽

Tumor Suppressor ◽

Long Noncoding Rna ◽

Noncoding Rna ◽

Proliferation Rate ◽

Expression Level ◽

The Novel ◽

Cell Proliferation Rate ◽

Potential Tumor Suppressor

Background/Aims: The novel long noncoding RNA (lncRNA) tumor suppressor candidate 7 (TUSC7) has been reported as a potential tumor suppressor, while the functional role of TUSC7 is still unknown in colorectal cancer (CRC). Here, we characterized TUSC7 expression profile in CRC patients and investigated its biological function and potential molecular mechanism. Methods: RNA isolation, qRT-PCR, cell counter kit-8 assay, cell cycle assay, EdU assay, and western blot were performed. Statistical analyses were performed using SPSS 18.0 software and p value < 0.05 was considered as statistically significant. Results: In a cohort of CRC patients, we found TUSC7 was significantly downregulated in CRC tissues compared with adjacent non-tumor tissues (P < 0.01). Patients with high expression of TUSC7 had better survival than those with low expression of TUSC7 (HR = 0.342, 95% CI: 0.120-0.972, P = 0.044). Cell count kit 8 and EdU assays showed that ectopic expression of TUSC7 in HCT116 and SW480 cells significantly inhibited cell proliferation rate. After silence of TUSC7 with small interfering RNA, cell proliferation rate increased. Flow cytometry analyses revealed cycles were arrested at G1 phase after TUSC7 overexpression. We found there were 2 binding sites of miR-211-3p within the sequence of TUSC7 and TUSC7 expression level was negatively correlated with miR-211-3p. TUSC7 overexpression increased the expression level of CDK6, which is a downstream target of miR-211-3p, in both RNA and protein level. Furthermore, luciferase reporter assay indicated that TUSC7 could sponge miR-211-3p. Conclusion: To summary, we demonstrated that TUSC7 is a potential tumor suppressor in CRC, and TUSC7 could inhibit CRC cell proliferation by completely sponging miR-211-3p.

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Temperature induces variations in the retinal cell proliferation rate in a cyprinid

Brain Research ◽

10.1016/s0006-8993(01)02804-9 ◽

2001 ◽

Vol 913 (2) ◽

pp. 190-194 ◽

Cited By ~ 7

Author(s):

Almudena Velasco ◽

Elena Cid ◽

Juana Ciudad ◽

Alberto Orfao ◽

Jose Aijon ◽

...

Keyword(s):

Cell Proliferation ◽

Proliferation Rate ◽

Retinal Cell ◽

Cell Proliferation Rate

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miR-9-5p Increases Sensitivity to Cisplatin in Thyroid Cancer Cells by Down-Regulating BRAF Expression

Journal of Biomaterials and Tissue Engineering ◽

10.1166/jbt.2019.2054 ◽

2019 ◽

Vol 9 (6) ◽

pp. 751-759

Author(s):

Wanzhi Chen ◽

Jichun Yu ◽

Rong Xie ◽

Meijun Zhong

Keyword(s):

Cell Proliferation ◽

Wound Healing ◽

Thyroid Cancer ◽

Cancer Cells ◽

Cell Apoptosis ◽

Cell Number ◽

Luciferase Reporter ◽

Reporter Assay ◽

Thyroid Cancer Cells ◽

Dual Luciferase Reporter Assay

Objective: To explore the expression of miR-9-5p and BRAF in cisplatin resistant strain thyroid cancer cells and reversal effect of drug resistance as well as the possible mechanism. Methods: The cisplatin-resistant thyroid cancer cells (FTC-133/DDP and TPC-1/DDP) were respectively divided into 3 groups as NC, DDP and DDP + miRNA groups. Measuring cell proliferation by MTT assay and cell apoptosis by flow cytometry; Evaluating invasion cell number and wound healing rates by transwell and wound healing assay. The relative proteins (BRAF, Mek and Erk1/2) were measured by WB assay. The correlation between miR-9-5p and BRAF by dual-luciferase reporter assay in FTC-133/DDP and TPC-1/DDP cells. Results: In FTC-133/DDP and TPC-1/DDP cells experiment, compared with DDP group, with miR-9-5p supplement, the cell proliferation rats were significantly depressed with cell apoptosis increasing (P < 0.001, respectively); invasion cell number and wound healing rats were significantly down-regulation (P < 0.001, respectively) in DDP + miRNA groups. Meanwhile, the BRAF, Mek and Erk1/2 proteins expressions were significantly depressed in DDP + miRNA groups were significantly suppressed compared with those in DDP groups (P < 0.001, respectively). By dual-luciferase reporter assay, BRAF was the target gene of miR-9-5p in FTC133/DDP and TPC-1/DDP cells. Conclusion: miR-9-5p increases sensitivity to cisplatin in thyroid cancer cells by down-regulating BRAF expression.

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