Regulation of collagen type I and biglycan mRNA levels by hormones and growth factors in normal and immortalized osteoblastic cell lines

2009 ◽  
Vol 9 (9) ◽  
pp. 1347-1354 ◽  
Author(s):  
D. Thiébaud ◽  
H.L. Guenther ◽  
A. Porret ◽  
P. Burckhardt ◽  
H. Fleisch ◽  
...  
2021 ◽  
Vol 11 (3) ◽  
pp. 560-566
Author(s):  
Bruce Chunsik Im ◽  
Junjun Li ◽  
Henok Kessete Afewerky ◽  
Xiaobing Jiang

Collagen type I α-1 chain (COL1A1) is closely involved in the advancement of various tumors, yet the role of COL1A1 in the progression of glioma is not clear. Herein, we evaluated the effect of COL1A1 on glioma cell proliferation. The effect of COL1A1 on glioma cell proliferation was assessed through overexpression or knockdown of COL1A1. The CCK-8 and colony formation assays, as well as immunohistochemistry (IHC) were used to detect COL1A1 expression in different glioma grades. U-87MG as well as U-251MG cells were stably-inserted with lentivirus containing COL1A1 through transfection, we additionally used qRT-PCR as well as Western blot assay to validate their overexpression efficiencies. COL1A1 mRNA and protein levels were upregulated in the high-grade glioma (HGG) compared to the low-grade glioma (LGG). COL1A1 IHC score was remarkably higher in HGG than LGG. The staining index (SI) further showed that COL1A1 protein levels were higher in HGG than LGG. The Kaplan–Meier analysis showed that elevated COL1A1 mRNA levels were obviously correlated with lower overall survival (OS) and disease-free survival (DFS) for brain glioma patients. COL1A1 mRNA and protein levels were markedly upregulated in human glioma cell lines when compared with brain astrocyte cell lines. The high expression level of COL1A1 facilitated glioma cell proliferation. COL1A1 knockdown remarkably inhibited glioma cell proliferation. Thus, this research shows that COL1A1 promotes glioma cell proliferation and is closely related to glioma prognosis.


Cells ◽  
2018 ◽  
Vol 7 (12) ◽  
pp. 246 ◽  
Author(s):  
Filippo Randelli ◽  
Alessandra Menon ◽  
Alessio Giai Via ◽  
Manuel Mazzoleni ◽  
Fabio Sciancalepore ◽  
...  

Background: Greater Trochanter Pain Syndrome (GTPS) is the main reason for recalcitrant lateral hip pain. Gluteus medius and minimus tendinopathy plays a key role in this setting. An injectable medical compound containing collagen type I (MD-Tissue, Guna) has been produced with the aim to counteract the physiological and pathological degeneration of tendons. In this study we aimed at characterizing the effect of this medical compound on cultured human gluteal tenocytes, focusing on the collagen turnover pathways, in order to understand how this medical compound could influence tendon biology and healing. Methods: Tenocytes were obtained from gluteal tendon fragments collected in eight patients without any gluteal tendon pathology undergoing total hip replacement through an anterior approach. Cell proliferation and migration were investigated by growth curves and wound healing assay, respectively. The expression of genes and proteins involved in collagen turnover were analysed by real-time PCR, Slot blot and SDS-zymography. Results: Our data show that tenocytes cultured on MD-Tissue, compared to controls, have increased proliferation rate and migration potential. MD-Tissue induced collagen type I (COL-I) secretion and mRNA levels of tissue inhibitor of matrix metalloproteinases (MMP)-1 (TIMP-1). Meanwhile, lysyl hydroxylase 2b and matrix metalloproteinases (MMP)-1 and -2, involved, respectively, in collagen maturation and degradation, were not affected. Conclusions: Considered as a whole, our results suggest that MD-Tissue could induce in tenocytes an anabolic phenotype by stimulating tenocyte proliferation and migration and COL-I synthesis, maturation, and secretion, thus favouring tendon repair. In particular, based on its effect on gluteal tenocytes, MD-Tissue could be effective in the discouraging treatment of GTPS. From now a rigorous clinical investigation is desirable to understand the real clinical potentials of this compound.


2017 ◽  
Vol 2017 ◽  
pp. 1-12 ◽  
Author(s):  
Xiaoyu Gu ◽  
Tingting Fang ◽  
Pinfang Kang ◽  
Junfeng Hu ◽  
Ying Yu ◽  
...  

Our study aimed firstly to observe whether ALDH2 was expressed in neonate rat cardiac fibroblasts, then to investigate the effect of activation of ALDH2 on oxidative stress, apoptosis, and fibrosis when cardiac fibroblasts were subjected to high glucose intervention. Cultured cardiac fibroblasts were randomly divided into normal (NG), NG + Alda-1, high glucose (HG), HG + Alda-1, HG + Alda-1 + daidzin, HG + daidzin, and hypertonic groups. Double-label immunofluorescence staining, RT-PCR, and Western blot revealed ALDH2 was expressed in cardiac fibroblasts. Compared with NG, ALDH2 activity and protein expression were reduced, and cardiac fibroblast proliferation, ROS releasing, 4-HNE protein expression, collagen type I and III at mRNA levels, and the apoptosis rate were increased in HG group. While in HG + Alda-1 group, with the increases of ALDH2 activity and protein expression, the cardiac fibroblast proliferation and ROS releasing were decreased, and 4-HNE protein expression, collagen type I and III at mRNA levels, and apoptosis rate were reduced compared with HG group. When treated with daidzin in HG + Alda-1 group, the protective effects were inhibited. Our findings suggested that ALDH2 is expressed in neonate rat cardiac fibroblasts; activation of ALDH2 decreases the HG-induced apoptosis and fibrosis through inhibition of oxidative stress.


2012 ◽  
Vol 303 (9) ◽  
pp. L778-L787 ◽  
Author(s):  
Jennifer J. P. Collins ◽  
Elke Kuypers ◽  
Ilias Nitsos ◽  
J. Jane Pillow ◽  
Graeme R. Polglase ◽  
...  

Chorioamnionitis and antenatal corticosteroids mature the fetal lung functionally but disrupt late-gestation lung development. Because Sonic Hedgehog (Shh) signaling is a major pathway directing lung development, we hypothesized that chorioamnionitis and antenatal corticosteroids modulated Shh signaling, resulting in an altered fetal lung structure. Time-mated ewes with singleton ovine fetuses received an intra-amniotic injection of lipopolysaccharide (LPS) and/or maternal intramuscular betamethasone 7 and/or 14 days before delivery at 120 days gestational age (GA) (term = 150 days GA). Intra-amniotic LPS exposure decreased Shh mRNA levels and Gli1 protein expression, which was counteracted by both betamethasone pre- or posttreatment. mRNA and protein levels of fibroblast growth factor 10 and bone morphogenetic protein 4, which are important mediators of lung development, increased 2-fold and 3.5-fold, respectively, 14 days after LPS exposure. Both 7-day and 14-day exposure to LPS changed the mRNA levels of elastin ( ELN) and collagen type I alpha 1 (Col1A1) and 2 (Col1A2), which resulted in fewer elastin foci and increased collagen type I deposition in the alveolar septa. Corticosteroid posttreatment prevented the decrease in ELN mRNA and increased elastin foci and decreased collagen type I deposition in the fetal lung. In conclusion, fetal lung exposure to LPS was accompanied by changes in key modulators of lung development resulting in abnormal lung structure. Betamethasone treatment partially prevented the changes in developmental processes and lung structure. This study provides new insights into clinically relevant prenatal exposures and fetal lung development.


1996 ◽  
Vol 80 (6) ◽  
pp. 2226-2233 ◽  
Author(s):  
M. Perhonen ◽  
X. Han ◽  
W. Wang ◽  
J. Karpakka ◽  
T. E. Takala

Skeletal muscle collagen expression was studied in normobaric sedentary (NS) and training (NT) and hypobaric sedentary (HS) and training (HT) rats after experimental periods of 10, 21, and 56 days. The weights of fast-twitch extensor digitorum longus (EDL) and slow-twitch soleus muscles were increased between the experimental period of 21 and 56 days so that EDL weight was 57 (P < 0.01) and 36% (P < 0.05) higher in 56 days HS (56HS) and 56 days HT (56HT), respectively, than in 56 days NS (56NS). Soleus muscle weight was higher in 56HS (61%; P < 0.01) and in 56HT (27%; P < 0.05) than in 56NT. In EDL muscle, collagen type I mRNA level was lower in 56HT than in 56NS (36%; P < 0.05) and 56NT (44%; P < 0.01). In 56HT, collagen type III mRNA level was 39 (P < 0.01) and 42% (P < 0.05) lower than in 56NS and 56HS, respectively. In soleus muscle, prolyl 4-hydroxylase activity was greater (P < 0.05) in 56NT, 56HS, and 56HT than in 56NS. Total hydroxyproline content in EDL muscle was increased in 56HS and 56HT and in soleus muscle of 56HS. In conclusion, although collagen types I and III mRNA levels in EDL muscle decreased in 56HT, the prolyl 4-hydroxylase data suggest unchanged synthesis of total collagen. Exposure to hypobaric conditions as such, its combination to endurance training, as well as training in normobaric conditions increased prolyl 4-hydroxylation capacity in soleus muscle, which may indicate respective change in collagen synthesis rate.


2004 ◽  
Vol 31 (9) ◽  
pp. 784-790 ◽  
Author(s):  
Gabor Fuerst ◽  
Gruber Reinhard ◽  
Stefan Tangl ◽  
Martina Mittlbock ◽  
Fidel Sanroman ◽  
...  

2002 ◽  
Vol 20 (3) ◽  
pp. 520-525 ◽  
Author(s):  
Tokifumi Majima ◽  
Ian K. Y. Lo ◽  
John A. Randle ◽  
Linda L. Marchuk ◽  
Nigel G. Shrive ◽  
...  

2018 ◽  
Vol 2018 ◽  
pp. 1-8
Author(s):  
Xuan Wang ◽  
Xia Li ◽  
Li-na Wang ◽  
Jing-juan Pan ◽  
Xue Yang ◽  
...  

Little is known about the effects of Buyang Huanwu decoction on pulmonary fibrosis. Herein, 144 healthy SD rats were randomly divided into six groups: blank control group (B), model control group (M), positive medicine control group (Mp), and high-, moderate-, and low-dose Buyang Huanwu decoction groups (Hd, Md, and Ld). A pulmonary fibrosis model was established by endotracheal injection of bleomycin. On the second day of modeling, the corresponding saline, methylprednisolone suspension, and the three doses of Buyang Huanwu decoction were used to treat the 6 groups of rats by intragastric administration for 7, 14, and 28 consecutive days. After 7, 14, and 28 days of treatment, the mRNA expression of CTGF and AKT, the protein level of CTGF, p-AKT, and collagen types I and III were tested. Finally, we found that the serum collagen type I and III level in Hd, Md, and Ld rats on the 14th and 28th day and the collagen type I and III level in Hd rats on 7th day were significantly lower than in M rats (P<0.01). The protein level of p-AKT and CTGF in Hd and Md rats on the 7th and 14th days and the protein level of p-AKT in Hd rats on the 28th day were lower than in M rats (P<0.01, P<0.05). The level of CTGF mRNA in Hd, Md, and Ld rats and the level of AKT mRNA in Hd and Md rats on the 7th, 14th, and 28th days and the expression level of AKT mRNA in Ld rats on the 14th and 28th days were significantly lower than in M rats (P<0.01). The study suggests that Buyang Huanwu decoction alleviated pulmonary fibrosis of rats by improvement of lung tissue morphology, low level of serum collagen types I and III, and the reduced expression of CTGF and p-AKT protein, which might be a result of its downregulated expression of CTGF and AKT mRNA levels.


Author(s):  
Joong Hyun Shim

Collagen type I production decreases with aging, leading to wrinkles and impaired skin function. Prostaglandin E2 (PGE2), a lipid-derived signaling molecule produced from arachidonic acid by cyclo-oxygenase, inhibits collagen production and induces matrix metallopeptidase 1 (MMP1) expression by fibroblasts in vitro. PGE2-induced collagen expression inhibition and MMP1 promotion are aging mechanisms. This study investigated the role of E-prostanoid 1 (EP1) in PGE2 signaling in normal human dermal fibroblasts (NHDFs). When EP1 expression was inhibited by EP1 small interfering RNA (siRNA), there were no significant changes in messenger RNA (mRNA) levels of collagen, type I, alpha 1 (COL1A1)/MMP1 between siRNA-transfected NHDFs and siRNA-transfected NHDFs with PGE2. This result showed that EP1 is a PGE2 receptor. Extracellular signal-regulated kinase 1/2 (ERK1/2) phosphorylation after PGE2 treatment significantly increased by ~2.5 times. In addition, PGE2 treatment increased the intracellular Ca2+ concentration in NHDFs. These results indicated that PGE2 is directly associated with EP1 pathway&ndash;regulated ERK1/2 and inositol trisphosphate (IP3) signaling in NHDFs.


Sign in / Sign up

Export Citation Format

Share Document