Thermoresponsive hydrogels based on a phosphorylated star-shaped copolymer: mimicking the extracellular matrix for in situ bone repair

2017 ◽  
Vol 5 (3) ◽  
pp. 428-434 ◽  
Author(s):  
Wei Wu ◽  
Zaifu Lin ◽  
Yanpeng Liu ◽  
Xinyuan Xu ◽  
Chunmei Ding ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Cell Proliferation ◽  
Bone Repair ◽  
Star Polymer ◽  
Thermoresponsive Hydrogels ◽  
Gel Transition

A bioinspired hydrogel prepared using a star-polymer exhibits sol to gel transition to induce in situ biomineralization and facilitate cell proliferation.

scholarly journals HtrA1 Is Specifically Up-Regulated in Active Keloid Lesions and Stimulates Keloids Development

2017 ◽  
Author(s):  
Satoko Yamawaki ◽  
Motoko Naitoh ◽  
Hiroshi Kubota ◽  
Rino Aya ◽  
Yasuhiro Katayama ◽  
...  
Keyword(s):  
Gene Expression ◽  
Extracellular Matrix ◽  
Cell Proliferation ◽  
In Situ Hybridization ◽  
Cell Surface ◽  
Western Blot ◽  
Blot Analysis ◽  
Normal Skin ◽  
Immunohistochemical Analysis

1) Background: Keloids occur after the failure during the wound-healing process, persist the inflammation and are refractory to various treatments. The pathogenesis of keloids is still unclear. We previously analyzed the gene expression profiles in keloid tissue using microarray and Northern blot analysis and found that HtrA1 was markedly upregulated in the keloid lesions. HtrA1 is a member of the HtrA family of serine protease, has been suggested to play a role in the pathogenesis of various diseases including age-related macular degeneration and osteoarthritis by modulating proteins in extracellular matrix or cell surface. We focused on HtrA1, analyzed the localization and the role in keloid pathogenesis. 2) Methods: Twenty seven keloid patients and seven unrelated patients were enrolled in this study. We performed in situ hybridization analysis, immunohistochemical analysis, western blot analysis and cell proliferation assay. 3) Results: First, the fibroblast-like cells expressed HtrA1 higher in the active keloid lesions than in the surrounding lesions in situ hybridization. Second, the proportion of HtrA1-positive cells in keloid was higher than that of in normal skin significantly in immunohistochemical analysis. Third, HtrA1 protein was up-regulated, relative to normal skin tissue samples in western blot analysis. Finally, silencing of HtrA1 gene expression suppressed the cell proliferation significantly. 4) Conclusion: HtrA1 was highly expressed in keloid tissues and the suppression of HtrA1 gene inhibited the proliferation of keloid-derived fibroblasts. HtrA1 may promote keloid development through accelerating cell proliferation and remodeling keloid-specific extracellular matrix or cell surface molecules. HtrA1 is suggested to have an important role in keloid pathogenesis.

In situ strategy for bone repair by facilitated endogenous tissue engineering

2015 ◽  
Vol 135 ◽  
pp. 581-587 ◽  
Author(s):  
Jingdi Chen ◽  
Yujue Zhang ◽  
Panpan Pan ◽  
Tiantang Fan ◽  
Mingmao Chen ◽  
...  
Keyword(s):  
Tissue Engineering ◽  
Bone Repair

P–543 Inhibition of cell proliferation and extracellular matrix formation in human uterine leiomyomas by 5-aza–2’-deoxycitidine via Wnt/ β-catenin pathway

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
M C Carbajo-García ◽  
A Corachán ◽  
M Segura ◽  
J Monleón ◽  
J Escrig ◽  
...  
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Extracellular Matrix ◽  
Cell Proliferation ◽  
Protein Expression ◽  
Hormonal Treatment ◽  
Dependent Manner ◽  
Dnmt Inhibitors ◽  
Qrt Pcr ◽  
Dose Dependent

Abstract Study question Is DNA methylation reversion through DNA methyltransferases (DNMT) inhibitors, such as 5-aza–2’-deoxycitidine, a potential therapeutic option for treatment of patients with uterine leiomyomas (UL)? Summary answer 5-aza–2’-deoxycitidine reduces proliferation and extracellular matrix (ECM) formation by inhibition of Wnt/ β-catenin pathway on UL cells, suggesting DNMT inhibitors as an option to treat UL. What is known already: UL is a multifactorial disease with an unclear pathogenesis and inaccurate treatment. Aberrant DNA methylation have been found in UL compared to myometrium (MM) tissue, showing hypermethylation of tumor suppressor genes, which contributes to the development of this tumor. The use of DNMT inhibitors, such as 5-aza–2’-deoxycytidine (5-aza-CdR), has been suggested to treat tumors in which altered methylation pattern is related to tumor progression, as occurs in UL. Based on this, we aimed to evaluate whether DNA methylation reversion through 5-aza-CdR reduces cell proliferation and ECM formation in UL cells, being a potential option for UL medical treatment. Study design, size, duration Prospective study comparing UL versus MM tissue and human uterine leiomyoma primary (HULP) cells treated with/without 5-aza-CdR at 0 µM (control), 2 µM, 5 µM and 10 µM for 72 hours. UL and MM tissue were collected from women without any hormonal treatment for the last 3 months (n = 16) undergoing myomectomy or hysterectomy due to symptomatic leiomyoma pathology. Participants were recruited between January 2019 and February 2020 at Hospital Universitario y Politecnico La Fe (Spain). Participants/materials, setting, methods Samples were collected from Caucasian premenopausal women aged 31–48 years, with a body mass index of < 30 and without hormonal treatment. DNMT1 gene expression was analysed in UL vs MM tissue by qRT-PCR and activity of DNMT was measured in UL and MM tissue and cells by ELISA. 5-aza-CdR effect on proliferation was assessed by CellTiter test and Western blot (WB), apoptosis and ECM analyzed by WB and Wnt/ β-catenin pathway by qRT-PCR and WB. Main results and the role of chance: DNMT1 gene expression was increased in UL compared to MM tissue (fold change [FC]=2.49, p-value [p]=0.0295). Similarly, DNMT activity was increased in both UL compared to MM tissue and HULP cells versus MM cells (6.50 vs 3.76 OD/h/mg, p = 0.026; 211.30 vs 63.67 OD/h/mg, p = 0.284, respectively). After 5-aza-CdR treatment, cell viability of HULP cells was reduced in a dose dependent manner, being statistically significant at 10 µM (85.25%, p = 0.0001). Accordantly, PCNA protein expression was significantly decreased at 10 µM in HULP cells (FC = 0.695, p = 0.034), demonstrating cell proliferation inhibition. Additionally, 5-aza-CdR inhibited ECM protein expression in HULP cells in a dose-dependent manner being statistically significant at 10 µM for COLLAGEN I (FC = 0.654, p = 0.023) and PAI–1 (FC = 0.654, p = 0.023), and at 2 µM and 10 µM for FIBRONECTIN (FC = 0.812, p = 0.020; FC = 0.733, p = 0.035; respectively). Final targets of Wnt/ β-catenin pathway were decreased after 5-aza-CdR treatment, protein expression of WISP1 was significantly inhibited at 10 µM (FC = 0.699, p = 0.026), while expression levels of Wnt/ β-catenin target genes C-MYC (FC = 0.745, p = 0.028 at 2 µM; FC = 0.728, p = 0.019 at 10 µM) and MMP7 (FC = 0.520, p = 0.003 at 5 µM, FC = 0.577, p = 0.007 at 10 µM) were also significantly downregulated in HULP-treated cells vs untreated cells. Limitations, reasons for caution: This study has strict inclusion criteria to diminish epigenetic variability, thereby we should be cautious extrapolating our results to general population. Besides, this is a proof of concept with the inherent cell culture limitations. Further studies are necessary to determine 5-aza-CdR dose and adverse effects on UL in vivo. Wider implications of the findings: 5-aza-CdR treatment reduces cell proliferation and ECM formation through Wnt/ β-catenin pathway inhibition, suggesting that inhibition of DNA methylation could be a promising new therapeutic approach to treat UL. Trial registration number Not applicable

Noninvasive Carcinoma of the Breast: Angiogenesis and Cell Proliferation

2004 ◽  
Vol 128 (8) ◽  
pp. 893-896 ◽  
Author(s):  
Ying Cao ◽  
Gladell P. Paner ◽  
Leonard B. Kahn ◽  
Prabha B. Rajan
Keyword(s):  
Cell Proliferation ◽  
Microvessel Density ◽  
Carcinoma In Situ ◽  
Nuclear Grade ◽  
Proliferation Index ◽  
Carcinoma Of The Breast ◽  
Cell Proliferation Index ◽  
Noninvasive Carcinoma ◽  
Mib 1

Abstract Context.—Angiogenesis and the cell proliferation index can predict the prognosis of invasive breast carcinoma; however, little is known of their roles in noninvasive tumor. Objective.—To investigate the correlation of microvessel density and cell proliferation index with other histologic parameters (histologic type, nuclear grade, and mitotic count) in 65 cases of noninvasive carcinoma of the breast. Design.—Formalin-fixed, paraffin-embedded tissues from 65 cases of carcinoma in situ of the breast were immunostained with antibody against factor VIII antigen and proliferation-associated nuclear antigen MIB-1. The microvessel density was measured by counting the total number of microvessels around the carcinoma in situ per 10 low-power microscopic fields. The cell proliferation index was calculated by counting MIB-1–positive nuclei in 100 tumor cells. A χ2 test and Spearman rank correlation test were used for statistical analysis. Results.—The microvessel density and cell proliferation index of comedo-type, high-nuclear-grade ductal carcinomas in situ are significantly higher than those of either noncomedo type ductal carcinomas in situ or lobular carcinoma in situ (P < .001). Conclusions.—Angiogenesis and the cell proliferation index are active biological processes and may be considered as markers to separate low- and high-risk patients with noninvasive breast carcinomas.

Contrasting patterns of c-myc and N-myc expression in proliferating, quiescent, and differentiating cells of the embryonic chicken lens

Development ◽  
1992 ◽  
Vol 115 (3) ◽  
pp. 813-820
Author(s):  
L.L. Harris ◽  
J.C. Talian ◽  
P.S. Zelenka
Keyword(s):  
Cell Proliferation ◽  
Protein Product ◽  
Mrna Levels ◽  
Lens Fiber ◽  
Proliferating Cells ◽  
Fiber Cells ◽  
Embryonic Chicken ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation

The present study uses the polymerase chain reaction and in situ hybridization to examine c-myc and N-myc mRNA in the embryonic chicken lens at 6, 10, 14 and 19 days of development and compares the pattern of expression obtained with the developmental pattern of cell proliferation and differentiation. In the central epithelium, c-myc mRNA levels were proportional to the percentage of proliferating cells throughout development. N-myc mRNA expression in this region was relatively low and showed no correlation with cell proliferation. The ratio of N-myc to c-myc mRNA increased markedly with the onset of epithelial cell elongation and terminal fiber cell differentiation, although both c-myc and N-myc mRNAs continued to be expressed in postmitotic, elongating cells of the equatorial epithelium and in terminally differentiating lens fiber cells. Thus, increased expression of N-myc, a gene whose protein product may compete with c-myc protein for dimerization partners, accompanies the dissociation of c-myc expression and cell proliferation during terminal differentiation of lens fiber cells.

NIR-II Ratiometric Lanthanide-Dye Hybrid Nanoprobes Doped Bioscaffolds for In Situ Bone Repair Monitoring

Nano Letters ◽  
2022 ◽  
Author(s):  
Peng Pei ◽  
Hongxing Hu ◽  
Ying Chen ◽  
Shangfeng Wang ◽  
Jing Chen ◽  
...  
Keyword(s):  
Bone Repair

scholarly journals Effect of bradykinin on renal mesangial cell proliferation and extracellular matrix secretion

2014 ◽  
Vol 13 (1) ◽  
pp. 490-498 ◽  
Author(s):  
C.Y. Liu ◽  
L.L. Zhou ◽  
Q. Cheng ◽  
S.N. Jiang ◽  
J. Sheng ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Cell Proliferation ◽  
Mesangial Cell ◽  
Mesangial Cell Proliferation ◽  
Extracellular Matrix Secretion

scholarly journals Cognate antigen engagement on parenchymal cells stimulates CD8+ T cell proliferation in situ

2017 ◽  
Vol 8 (1) ◽  
Author(s):  
Robyn M. Sutherland ◽  
Sarah L. Londrigan ◽  
Jamie L. Brady ◽  
Emma M. Carrington ◽  
Julia M. Marchingo ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
T Cell ◽  
Cd8 T Cell ◽  
T Cell Proliferation ◽  
Cognate Antigen ◽  
Parenchymal Cells
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