scholarly journals Buyang Huanwu Decoction Ameliorates Bleomycin-Induced Pulmonary Fibrosis in Rats via Downregulation of Related Protein and Gene Expression

2018 ◽  
Vol 2018 ◽  
pp. 1-8
Author(s):  
Xuan Wang ◽  
Xia Li ◽  
Li-na Wang ◽  
Jing-juan Pan ◽  
Xue Yang ◽  
...  
Keyword(s):  
Pulmonary Fibrosis ◽  
Protein Level ◽  
Collagen Type ◽  
Collagen Type I ◽  
Control Group ◽  
Type I ◽  
Mrna Levels ◽  
Collagen Types ◽  
Buyang Huanwu Decoction ◽  
Serum Collagen

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.

Losartan attenuates paraquat-induced pulmonary fibrosis in rats

2014 ◽  
Vol 34 (5) ◽  
pp. 497-505 ◽  
Author(s):  
F Guo ◽  
YB Sun ◽  
L Su ◽  
S Li ◽  
ZF Liu ◽  
...  
Keyword(s):  
Pulmonary Fibrosis ◽  
Lung Injury ◽  
Mrna Expression ◽  
Collagen Type ◽  
Collagen Type I ◽  
Control Group ◽  
Type I ◽  
Expression Levels ◽  
Relative Expression ◽  
Tgf Β1

Paraquat (PQ) is one of the most widely used herbicides in the world and can cause pulmonary fibrosis in the cases with intoxication. Losartan, an angiotensin II type 1 receptor antagonist, has beneficial effects on the treatment of fibrosis. The aim of this study was to examine the effect of losartan on pulmonary fibrosis in PQ-intoxicated rats. Adult male Sprague Dawley rats ( n = 32, 180–220 g) were randomly assigned to four groups: (i) control group; (ii) PQ group; (iii) PQ + losartan 7d group; and (iv) PQ + losartan 14d group. Losartan treatment (intragastrically (i.g.), 10 mg/kg) was performed for 7 and 14 days after a single i.g. dose of 40 mg/kg PQ. All rats were killed on the 16th day, and hematoxylin–eosin and Masson’s trichrome staining were used to examine lung injury and fibrosis. The levels of hydroxyproline and transforming growth factor β1 (TGF-β1), matrix metallopeptidase 9 (Mmp9), and tissue inhibitor of metalloproteinase 1 (TIMP-1) messenger RNA (mRNA) expression and relative expression levels of collagen type I and III were also detected. PQ caused a significant increase in hydroxyproline content, mRNA expression of TGF-β1, Mmp9, and TIMP-1, and relative expression levels of collagen type I and III (  p < 0.05), while losartan significantly decreased the amount of hydroxyproline and downregulated TGF-β1, Mmp9, and TIMP-1 mRNA and collagen type I and III expressions (  p < 0.05). Histological examination of PQ-treated rats showed lung injury and widespread inflammatory cell infiltration in the alveolar space and pulmonary fibrosis, while losartan could markedly reduce such damage and prevent pulmonary fibrosis. The results of this study indicated that losartan could reduce lung damage and prevent pulmonary fibrosis induced by PQ.

P0650URINE PEPTIDOME ANALYSIS IN HEART FAILURE, CHRONIC KIDNEY DISEASE AND CARDIORENAL SYNDROME TOWARDS THE DEFINITION OF DISEASE-SPECIFIC MARKERS

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Eleni Petra ◽  
Tianlin He ◽  
Agnieszka Latosinska ◽  
Rafael Stroggilos ◽  
Harald Mischak ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Collagen Type ◽  
Cardiorenal Syndrome ◽  
Collagen Type I ◽  
Type I ◽  
Collagen Types ◽  
Alpha 1 Antitrypsin ◽  
Urinary Peptides

Abstract Background and Aims The cardiorenal syndrome (CRS) reflects the complex interplay between kidney and heart diseases, but its molecular basis remains poorly understood. Multiple studies have demonstrated the association of urinary biomarkers with both heart and kidney diseases. However, their relevance and involvement in CRS have not been investigated yet. To address this gap, a study was designed with the aim to compare urinary biomarkers specific for heart failure (HF) and chronic kidney disease (CKD) with peptides representing CRS, with the ultimate target to connect these findings towards a better understanding of CRS pathophysiology. Method A total of 3.463 urinary peptidomic datasets from patients with HF, CKD, or with both HF and CKD (CRS) as well as patients with no apparent diseases (controls) were retrieved and analyzed from the urinary peptidomics database (Latosinska A et al., Electrophoresis 2019; 40: 2294-2308). Following the matching for age, gender, heart and kidney function, differences in the abundance of urinary peptides were investigated in a cohort comprised of 390 patients with HF, 257 patients with CKD, 392 patients with CRS and 356 controls. The non-parametric Mann-Whitney U test was applied, followed by correction for multiple testing using the Benjamini-Hochberg method. To map the peptides to the protein precursor, the alignment tool Geneious (www. geneious.com) was applied, while the PeptideRanker (http://distilldeep.ucd.ie/PeptideRanker/) was used to predict probability of peptide being bioactive. Results The multiple pair-wise comparisons resulted in the identification of numerous differentially abundant peptides (p&lt;0.05) between the studied conditions, including among others 176 HF-specific, 146 CKD-specific and 35 CRS-specific peptides. Among the HF-specific peptides, the majority (n=94, 53.4%) originated from collagen type I, II and III. In the case of CKD-specific peptides, 24 (16.43%) originated from alpha-1-antitrypsin, 19 (13.0%) from b2-microglobulin and 15 (10.27%) from collagen type I. For the CRS specific peptides, fragments of Ig lambda-2 chain C regions (n=4, 11.42%), collagen type III (n=4, 11.42%), secreted and transmembrane protein 1 (n=3, 8.57%) and gelsolin (n=1, 2.85%) were identified (figure: 1). Of the 176 HF-specific peptides, 94 (53.40%) were predicted as bioactive, including, among others, fragments of collagen types I (n=43, 45.74%) and III (n=21, 22.34%). In the former, peptides with the higher bioactivity scores were aligned close to the N terminus of the precursor protein, whereas in the latter, peptides were in close proximity to both N and C termini. Along the same lines, 32 (21.91%) of the 146 CKD-specific peptides were predicted as bioactive, including peptides from collagen types I and III with the highest score, as well as fragments from collagen type V and the C terminus of the b2-microglobulin and alpha-1-antitrypsin proteins. No CRS-specific peptides could be predicted as bioactive. Conclusion Specific urinary peptides significantly associated with CRS, but not with HF or CKD, could be identified. These data indicate that on a molecular level, CRS is not merely the result of a combination of HF and CKD, but may represent a distinct pathology, defined via specific proteomic changes. It is expected that interpretation of these findings in the context of existing literature as well as in vitro activity assays will help to understand their biological relevance in CRS.

scholarly journals Biofabrication of SDF-1 Functionalized 3D-Printed Cell-Free Scaffolds for Bone Tissue Regeneration

2020 ◽  
Vol 21 (6) ◽  
pp. 2175 ◽  
Author(s):  
Alina Lauer ◽  
Philipp Wolf ◽  
Dorothea Mehler ◽  
Hermann Götz ◽  
Mehmet Rüzgar ◽  
...  
Keyword(s):  
Bone Regeneration ◽  
Bone Tissue ◽  
Tissue Regeneration ◽  
Bone Growth ◽  
Collagen Type ◽  
Biomechanical Testing ◽  
Collagen Type I ◽  
Bone Tissue Regeneration ◽  
Control Group ◽  
Type I

Large segmental bone defects occurring after trauma, bone tumors, infections or revision surgeries are a challenge for surgeons. The aim of our study was to develop a new biomaterial utilizing simple and cheap 3D-printing techniques. A porous polylactide (PLA) cylinder was printed and functionalized with stromal-derived factor 1 (SDF-1) or bone morphogenetic protein 7 (BMP-7) immobilized in collagen type I. Biomechanical testing proved biomechanical stability and the scaffolds were implanted into a 6 mm critical size defect in rat femur. Bone growth was observed via x-ray and after 8 weeks, bone regeneration was analyzed with µCT and histological staining methods. Development of non-unions was detected in the control group with no implant. Implantation of PLA cylinder alone resulted in a slight but not significant osteoconductive effect, which was more pronounced in the group where the PLA cylinder was loaded with collagen type I. Addition of SDF-1 resulted in an osteoinductive effect, with stronger new bone formation. BMP-7 treatment showed the most distinct effect on bone regeneration. However, histological analyses revealed that newly formed bone in the BMP-7 group displayed a holey structure. Our results confirm the osteoinductive character of this 3D-biofabricated cell-free new biomaterial and raise new options for its application in bone tissue regeneration.

scholarly journals Effect of a Collagen-Based Compound on Morpho-Functional Properties of Cultured Human Tenocytes

Cells ◽  
2018 ◽  
Vol 7 (12) ◽  
pp. 246 ◽  
Author(s):  
Filippo Randelli ◽  
Alessandra Menon ◽  
Alessio Giai Via ◽  
Manuel Mazzoleni ◽  
Fabio Sciancalepore ◽  
...  
Keyword(s):  
Matrix Metalloproteinases ◽  
Collagen Type ◽  
Clinical Investigation ◽  
Pain Syndrome ◽  
Collagen Type I ◽  
Type I ◽  
Mrna Levels ◽  
Collagen Turnover ◽  
And Migration ◽  
Proliferation And Migration

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.

scholarly journals Lysyl hydroxylation in collagens from hyperplastic callus and embryonic bones

1992 ◽  
Vol 282 (2) ◽  
pp. 313-318 ◽  
Author(s):  
H W Lehmann ◽  
M Bodo ◽  
C Frohn ◽  
A Nerlich ◽  
D Rimek ◽  
...  
Keyword(s):  
Fetal Development ◽  
Bone Repair ◽  
Callus Tissue ◽  
Collagen Type ◽  
Compact Bone ◽  
Collagen Type I ◽  
Postnatal Period ◽  
Type I ◽  
Collagen Types ◽  
Hyperplastic Callus

Tissue from two patients with osteogenesis imperfecta suffering from a hyperplastic callus was studied. Although collagen type I from the compact bone and the skin and fibroblast cultures of these patients showed normal lysyl hydroxylation, collagen types I, II, III and V from the callus tissue were markedly overhydroxylated. Furthermore, the overhydroxylation of lysine residues covered almost equally the entire alpha 1 (I) collagen chain, as demonstrated by the analysis of individual CNBr-derived peptides. In addition, collagen type I was isolated from femoral compact bone of 33 individuals who died between the 16th week of gestational age and 22 years. Lysyl hydroxylation rapidly decreased in both collagen alpha 1 (I) and alpha 2 (I) chains during fetal development, and only little in the postnatal period. The transient increase in lysyl hydroxylation and the involvement of various collagen types in callus tissue argue for a regulatory mechanism that may operate in bone repair and during fetal development.

Immunohistochemical Localization of Collagen Types I, III, and IV, Laminin, Fibronectin, and Keratin in the Endolymphatic Sac

2000 ◽  
Vol 109 (2) ◽  
pp. 180-186 ◽  
Author(s):  
Teruhiko Harada ◽  
Youngki Kim ◽  
Steven K. Juhn ◽  
Yasuo Sakakura
Keyword(s):  
Collagen Type ◽  
Collagen Type I ◽  
Immunohistochemical Localization ◽  
Basement Membranes ◽  
Endolymphatic Sac ◽  
Type I ◽  
Collagen Types ◽  
Type Iv ◽  
Baseline Information ◽  
Subepithelial Layer

We have employed immunohistochemistry to obtain baseline information on the molecular constituents of the extracellular matrix (ECM) of the endolymphatic duct (ED) and endolymphatic sac (ES) of the chinchilla. The results demonstrated that collagen types I and III were distributed in the subepithelial layer in the ED and ES, type IV collagen and laminin in the basement membranes, and fibronectin in the subepithelial layer and partly in the conglomerated cells in the ES. Collagen type III was diffusely distributed in the whole subepithelial layer of the ES, whereas collagen type I was concentrated densely in the deep layer of the interstitium, although gradually, the cuboidal epithelium in the ES was transformed into a flatter type in the ED. The epithelial cells of the ED and ES were clearly positive for keratin. This study deals, in particular, with the normal distribution of ECM components of the ED and ES of the chinchilla.

Relaxin attenuates silica-induced pulmonary fibrosis by regulating collagen type I and MMP-2

2013 ◽  
Vol 17 (3) ◽  
pp. 537-542 ◽  
Author(s):  
Xiao-Feng Li ◽  
Jing Liao ◽  
Zhi-Qiang Xin ◽  
Wen-Qing Lu ◽  
Ai-Lin Liu
Keyword(s):  
Pulmonary Fibrosis ◽  
Collagen Type ◽  
Collagen Type I ◽  
Type I

scholarly journals Effect of ALDH2 on High Glucose-Induced Cardiac Fibroblast Oxidative Stress, Apoptosis, and Fibrosis

2017 ◽  
Vol 2017 ◽  
pp. 1-12 ◽  
Author(s):  
Xiaoyu Gu ◽  
Tingting Fang ◽  
Pinfang Kang ◽  
Junfeng Hu ◽  
Ying Yu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protein Expression ◽  
High Glucose ◽  
Collagen Type ◽  
Cardiac Fibroblasts ◽  
Collagen Type I ◽  
Cardiac Fibroblast ◽  
Type I ◽  
Mrna Levels ◽  
Neonate Rat

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.

Diagnosis of bone metastasis in patients with lung cancer using urinary and serum collagen type I telopeptide (NTx).

2011 ◽  
Vol 29 (15_suppl) ◽  
pp. e18044-e18044
Author(s):  
H. Okada ◽  
M. Tamiya ◽  
S. Tokunaga ◽  
H. Daga ◽  
K. Taira ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Bone Metastasis ◽  
Collagen Type ◽  
Collagen Type I ◽  
Type I ◽  
Serum Collagen ◽  
Diagnosis Of Bone Metastasis
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