Connective Tissue Proteins Research Articles

T cells and orbital connective tissue in endocrine orbitopathy.

In order to analyse the immunological changes in patients with endocrine orbitopathy (EO) the antigenic character of orbital connective tissue was studied. Counter-stimulation assays of patients' lymphocytes with autologous retrobulbar fibroblasts resulted in a markedly increased lymphocyte proliferation in comparison to incubation with retrobulbar control fibroblasts. Proliferation tests of retrobulbar T cell lines showed significant responses to autologous retro-orbital connective tissue proteins, with molecular weights of 6-10 kD and 19-26 kD. Phenotypic analysis of orbital T cell lines indicates that they consisted predominantly of CD4+ cells. Hyaluronic acid production of orbital fibro blasts following co-cultivation with lymphocytes of EO patients or controls revealed a threefold increased synthesis in patients with EO. Furthermore, distribution pattern of orbital extracellular matrix glycosaminoglycans (GAG) differs in EO patients in comparison to controls. The results suggest the presence of autoreactive T cells directed against antigens of orbital fibroblasts, whose stimulation results in an augmented GAG synthesis in patients with EO.

New polypeptide conformations and their roles in molecular diseases of the vascular wall

New polypeptide conformations are described in which the repeating unit contains intrarepeat hydrogen bonding and in which there may or may not be hydrogen bonding between the repeating units. These conformations, called β spirals, were derived from polymers of repeat peptides of elastin, the connective tissue protein of the core of the elastic fiber. It is argued that these β spirals associate to form supramolecular fibrous constructs by intermolecular hydrophobic interactions and that these structures, which contain preferred though dynamic secondary structure, form elastomeric fibers which are not random. An appropriate understanding of these structures and their important biological properties require analysis from the disciplines of quantum chemistry, statistical mechanics, and the theory of rate processes. The manner in which these β-spirals associate, which is fundamental to the mechanism of fiber formation, provides insights into the molecular pathology of the vascular wall, specifically into the disruptive effects of decreased temperature, of lipid deposition, and of pathological calcification.

Genetic and orthopedic aspects of collagen disorders

'Collagens' are a family of structurally related proteins that play a wide variety of roles in the extracellular matrix. To date, there are at least 29 known types of collagen. Accordingly, abnormality in the various collagens produces a large category of diseases with heterogeneous symptoms. This review presents genetic and orthopedic aspects of type II, IX, and XI collagen disorders. Although a diverse group of conditions, mutation of collagens affecting the articular cartilage typically produces an epiphyseal skeletal dysplasia phenotype. Often, the ocular or auditory systems or both are also involved. Treatment of these collagenopathies is symptomatic and individualized. Study of tissue from animal models allows examination of mutation effects on the abnormal protein structure and function. The collagen superfamily comprises an important structural protein in mammalian connective tissue. Mutation of collagens produces a wide variety of genetic disorders, and those mutations affecting types II, IX, and XI collagens produce an overlapping spectrum of skeletal dysplasias. Findings range from lethal to mild, depending on the mutation of the collagen gene and its subsequent effect on the structure and/or metabolism of the resultant procollagen and/or collagen protein and its function in the body.

Влияние гормона роста человека на состояние коллагена в области повреждения кожи крыс

Investigation of opportunities to affect the synthesis of collagen is of current importance to surgery as the synthesis of extracellular matrix collagen is the constituent of wound healing, which determines the rate and quality of tissue restoration. Growth hormone is one of the factors influencing the synthesis of the major protein of connective tissue - collagen. We have hypothesized that after making a subcutaneous wound, by impairing the basement membrane integrity, and by causing skin defect resolution, a recombinant human growth hormone (rh GH) preparation may affect the starting synthesis of an extracellular collagen matrix. An electric dermatome was used for partial skin thickness damage. The experimental animals - Wistar rats were randomized into two groups. The experimental group received subcutaneous rhGH injections (2.0 mg/kg) every day. The control group was daily given subcutaneous placebo injections. Wound tissue histomorphometry was used to estimate the area of the dermal fibrillary collagen network, the number of fascicles and the length of their perimeter and to calculate the volume of the fibrillary collagen network. There were both a statistically significant prevalence of collagen synthesis in the matrix of a wound on days 3, 6, 9 (66.55tl2.65, 64.23±7.19, and 65.74±8.I8) versus (51.32+- 14.85; 52.77+-2.41 , and 61.53±9.35), respectively, and signs of early mature connective tissue formation in the region of partial skin thickness damage in the rats receiving rh GH injections, which manifested as fewer collagen fibrils (156.23±5.53 and 166.14±4.24 to 143.34±2.90) as compared with the controlgroup (200.13±4.6S and 193.79+-.5.35 to I54.14±5.42, respectively).

Abstract 1769: Caveolin-1 Regulates TGF-Beta Signaling in Cardiac Remodeling

In cardiac fibrosis, fibrous tissue replaces healthy contractile tissue. The regulation of these processes is controlled in large part by transforming growth factor-β (TGF-β). Caveolin-1 (cav1) regulates TGF-β signaling by either sequestering the TGF-β receptor complex or enhancing its degradation. Thus, cav1 may prevent TGF-β directed fibrosis. To investigate the role of cav1 in cardiac remodeling, we performed left ventricular cryoinjury in Cav1-deficient (Cav1−/−) mice and wild-type controls. Ventricular function was followed by echocardiography, and 3, 14, and 30 days after surgery, cardiac RNA and protein were analyzed for inflammatory responses, connective tissue and TGF-β signaling related proteins. Cryoinjured WT presented reduced cav1 expression. Concurrently, evidence of activation of TGF-β signaling was measured as shown by increase of Smad2 phosphorylation. Moreover Cav1−/− cryoinjured hearts had enhanced Smad2 phosphorylation. Collagen gene expression was transiently upregulated in cryoinjured WT mice 3 days post surgery (2.5-fold) and this elevation persisted in Cav1−/− hearts (3.5-fold at 14 days). The level of collagenases (mmp-8 and -13) expression was dramatically increased in the 3-day cryoinjured WT but not in Cav1−/− mice. As a result, augmented collagen deposition, resulting from increased collagen expression and reduced degradation by collagenases, was observed by Masson’s trichrome and picrosirius staining in injured Cav1−/− hearts. WT mice had a transient decline in fractional shortening (FS) but function returned to baseline by 30 days post-injury. In contrast, cryoinjured Cav1−/− mice had a significant lower % FS after 30 days compared to baseline or to cryoinjured WT (67.4 ± 9.6, 76 ± 11, 76.9 ± 5.5, respectively). Moreover Cav1−/− mice presented an altered inflammatory response following cryoinjury. Reduced macrophage infiltrates and IL-6 level of expression were also measured in cryoinjured Cav1−/− mice. These data indicate that in absence of caveolae, TGF-β signaling is enhanced, and this leads to a disordered inflammatory response and suboptimal cardiac remodeling that may impair left ventricular function.

Epithelial to Mesenchymal Transformation in Tubular Epithelial Cells Undergoing Anoxia

Aim Epithelial–mesenchymal transformation (EMT) has been proved to be a critical event in fibrogenesis of renal allografts. This study sought to determine whether anoxia could induce EMT from tubular epithelial cells (TEC). Methods Rat TEC-line (NRK-52E) was cultured in Dulbelco's modified Eagle's medium (DMEM) without glucose under 100% N 2 for 4 hours. After 6, 12, 24, 48, and 72 hours, the expressions of connective tissue growth factor (CTGF) mRNA and protein were measured by real-time RT-PCR and Western blot, respectively. Morphologic changes and cytoskeleton remodeling were observed in NRK-52E cells under laser confocal microscopy. Immunohistochemistry and flow cytometry were used to detect expression changes of E-cadherin, α-smooth muscle actin (SMA), types I and IV collagen, all of which are involved in TEC, EMT. Results After stimulation by anoxia, NRK-52E cells became round and enlarged with a remodeled cytoskeleton. The expressions of CTGF mRNA and protein were upregulated after 6 hours, reaching their peak at 48 hours. The expressions of types I and IV collagen, and α-SMA were all upregulated except for E-cadherin. Conclusions Anoxia upregulated the expression of CTGF and other EMT-associated genes in NRK-52E cells.

Prediction of 3-Dimensional Structure of Cathepsin L Protein of Rattus Norvegicus

Cathepsin L is a cysteine protease which degrades connective tissue proteins like collagen, elastin and fibronectin. Increase in the expression of cathepsin L in aged kidney leading to considerable loss of organ function in old age. Recently it has been reported that SARS-CoV or SARS-CoV spike protein-pseudotyped retroviruses utilize the enzymatic activity of endosomal cathepsin L protease for viral entry. A 3D structure of rat cathepsin L was constructed in this report through homology modeling using the X-ray structure of procathepsin L from Homo sapiens (PDB code: 1CS8). The homology modeling was done by using the MODELLER 9v2 software. The final model obtained by molecular mechanics and dynamics method and was assessed by PROCHECK and VERIFY 3D graph, which showed that the final refined model is reliable. The model could be further explored for characterizing the protein.

Antioxidative activity of rosemary extract using connective tissue proteins as carriers

SummaryIn the research the activity of rosemary extract introduced using connective tissue proteins was investigated, taking into consideration the effect of the type of carrier (collagen and elastin), carrier concentration (1%, 2%, 4%) and the method of its introduction to fat substrate (rehydrated or unhydrated). Antioxidative activity was assessed using the Oxidograph instrumental test. The activity of rosemary extract on protein preparations was significantly affected by the rehydration of these preparations. The application of collagen as carrier of rosemary extract had an advantageous effect on the activity of this antioxidant. In turn, under the adopted testing conditions the application of elastin resulted in partial masking of antioxidative activity of rosemary extract. Amounts of the carriers, onto which the antioxidant was introduced, did not have a statistically significant effect on this activity.

Raman Spectroscopy for Monitoring Protein Structure in Muscle Food Systems

Raman spectroscopy offers structural information about complex solid systems such as muscle food proteins. This spectroscopic technique is a powerful and a non-invasive method for the study of protein changes in secondary structure, mainly quantified, analysing the amide I (1650–1680 cm− 1) and amide III (1200–1300 cm− 1) regions and C-C stretching band (940 cm− 1), as well as modifications in protein local environments (tryptophan residues, tyrosil doublet, aliphatic aminoacids bands) of muscle food systems. Raman spectroscopy has been used to determine structural changes in isolated myofibrillar and connective tissue proteins by the addition of different compounds and by the effect of the conservation process such as freezing and frozen storage. It has been also shown that Raman spectroscopy is particularly useful for monitoring in situ protein structural changes in muscle food during frozen storage. Besides, the possibilities of using protein structural changes of intact muscle to predict the protein functional properties and the sensory attributes of muscle foods have been also investigated. In addition, the application of Raman spectroscopy to study changes in the protein structure during the elaboration of muscle food products has been demonstrated.

Down-regulation of Caveolin-1, an Inhibitor of Transforming Growth Factor-β Signaling, in Acute Allergen-induced Airway Remodeling

Asthma can progress to subepithelial airway fibrosis, mediated in large part by transforming growth factor-beta (TGF-beta). The scaffolding protein caveolin-1 (cav1) can inhibit the activity of TGF-beta, perhaps by forming membrane invaginations that enfold TGF-beta receptors. The study goals were 1) to evaluate how allergen challenge affects lung expression of cav1 and the density of caveolae in vivo 2) to determine whether reduced cav1 expression is mediated by interleukin (IL)-4 and 3) to measure the effects of decreased expression of cav1 on TGF-beta signaling. C57BL/6J, IL-4-deficient mice, and cav1-deficient mice, sensitized by intraperitoneal injections of phosphate-buffered saline or ovalbumin (OVA) at days 0 and 12, received intranasal phosphate-buffered saline or OVA challenges at days 24, 26, and 28. Additionally, another group of C57BL/6J mice received IL-4 by intratracheal instillation for 7 days. We confirmed that the OVA-allergen challenge increased eosinophilia and T-helper type 2-related cytokine levels (IL-4, IL-5, and IL-13) in bronchoalveolar lavage. Allergen challenge reduced lung cav1 mRNA abundance by 40%, cav1 protein by 30%, and the number of lung fibroblast caveolae by 50%. Administration of IL-4 in vivo also substantially decreased cav1 expression. In contrast, the allergen challenge did not decrease cav1 expression in IL-4-deficient mice. The reduced expression of cav1 was associated with activation of TGF-beta signaling that was further enhanced in OVA-sensitized and challenged cav1-deficient mice. This study demonstrates a previously unknown modulation of TGF-beta signaling by IL-4, via cav1, suggesting novel therapeutic targets for controlling the effects of TGF-beta and thereby ameliorating pathological airway remodeling.

In vitro hypoxia increases production of matrix metalloproteinases and tryptase in isolated rat lung mast cells

Chronic hypoxia results in hypoxic pulmonary hypertension characterized by fibrotization and muscularization of the walls of peripheral pulmonary arteries. This vessel remodeling is accompanied by an increase in the amount of lung mast cells (LMC) and the presence of small collagen cleavage products in the vessel walls. We hypothesize that hypoxia activates LMC, which release matrix metalloproteinases (MMPs) cleaving collagen and starting increased turnover of connective tissue proteins. This study was designed to determine whether in vitro hypoxia stimulates production of MMPs in rat LMC and increases their collagenolytic activity. The LMC were separated on the Percoll gradient and then were divided into two groups and cultivated for 24 h in 21 % O(2) + 5 % CO(2) or in 10 % O(2) + 5 % CO(2). Presence of the rat interstitial tissue collagenase (MMP-13) in LMC was visualized by immunohistological staining and confirmed by Western blot analysis. Total MMPs activity and tryptase activity were measured in both cultivation media and cellular extracts. Exposure to hypoxia in vitro increased the amount of cells positively labeled by anti-MMP-13 antibody as well as activities of all measured enzymes. The results therefore support the concept that LMC are an important source of increased collagenolytic activity in chronic hypoxia.

Prepubertal onset of diabetes prevents expression of renal cortical connective tissue growth factor

Puberty unmasks or accelerates the nephropathy of diabetes mellitus (DM). We performed focused microarray analysis to test the hypothesis that one or more genes in the transforming growth factor beta (TGF-beta) signaling system would be differentially regulated in male rats depending on their age at onset of DM. Littermates were started on the 6-week protocol at 4 weeks or 14 weeks of age. Renal cortical RNA was isolated and analyzed using gene chips with more than 30,000 transcripts. Age-specific effects of DM were demonstrated for 1,760 transcripts. Analysis then focused on 89 genes involved in the TGF-beta signaling pathway. Three of these genes showed age-dependent responses to DM, confirmed by quantitative real-time reverse transcriptase-polymerase chain reaction (RT-PCR). Connective tissue growth factor (CTGF) mRNA and protein were both increased approximately 30% in the renal cortex 6 weeks after adult-onset DM, with no alteration in either parameter after juvenile onset. Follistatin and avian myelocytomatosis viral oncogene homolog mRNA both showed a similar age-related pattern of response to DM, but protein levels did not parallel mRNA for either of these gene products. Given the known roles of CTGF in progressive nephropathies, it is an attractive candidate to explain pubertal acceleration or unmasking of the kidney disease of diabetes.

Effect of compound Biejia Ruangan tablet on expressions of connective tissue growth factor mRNA and protein in kidney tissue of rats with adriamycin-induced nephropathy

To investigate the changes of connective tissue growth factor (CTGF) protein and CTGF mRNA in kidney tissue of rats with adriamycin (ADR)-induced nephropathy and to study the effects of compound Biejia Ruangan tablet (CBJRGT), a traditional Chinese herbal medicine for treatment of liver fibrosis. A rat model of ADR-induced nephropathy after one-sided nephrectomy was established. Forty-five Wistar rats were randomly divided into 5 groups: normal control group, sham-operated group, untreated group, lotensin-treated group and CBJRGT-treated group. Pathological changes of the kidney tissue were observed by microscopy after 10-week drug administration. The expressions of CTGF protein and CTGF mRNA in the kidney tissue were measured by the methods of immunohistochemistry and in situ hybridization. The expressions of CTGF protein and CTGF mRNA in the normal and sham-operated groups were decreased in the intracytoplasm of glomerular mesangial cells, renal tubular epithelial cells and interstitial cells. Compared with the sham-operated group, the expressions of CTGF protein and CTGF mRNA in the untreated group were markedly increased and the development of renal fibrosis in the untreated group could be observed. CBJRGT could significantly decrease the expressions of CTGF protein and CTGF mRNA, and there was no significant difference between CBJRGT-treated group and lotensin-treated group. CBJRGT may suppress the development of fibrosis through down-regulating the expressions of CTGF protein and CTGF mRNA.

Study of the hypoxia-dependent regulation of human CYGB gene

Cytoglobin (CYGB) is ubiquitously expressed in all tissues and has been characterized as a respiratory protein in connective tissues. CYGB is up-regulated during hypoxia, implicating its function in maintaining the homeostasis redox of the cell. Here, we study the underlying molecular mechanisms by which hypoxia regulates human CYGB gene expression. When cells were subjected to hypoxia, the expression of endogenous CYGB was up-regulated ∼1.7-fold in BEAS-2B cells ( p ⩽ 0.05) and ∼1.6-fold in HeLa cells ( p ⩽ 0.05). Dual-luciferase assays and site directed mutagenesis showed the presence of hypoxia responsive elements (HREs) at positions −141, −144 and −448 that were essential for activation of CYGB expression under hypoxic conditions. The binding of hypoxia inducible factor (HIF-1) protein to the HREs was confirmed by gel shift and chromatin immunoprecipitation (ChIP) assays. These results indicate that HRE motifs are directly involved in the activation of the CYGB transcription under hypoxia.

The structural and functional consequences of chronic allergic inflammation of the airways.

Although asthma is generally considered a form of reversible airway obstruction, there is evidence that chronic allergic inflammation can lead to structural changes in the airway and a degree of progressive fixed airway obstruction. More importantly, these structural changes can lead to airway hyper-responsiveness. The structural consequences of chronic allergic inflammation are secondary to cellular proliferation and reorganization of the connective tissue constituents of the airway wall. Smooth muscle proliferation and hypertrophy may increase the potential for smooth muscle shortening against the elastic loads provided by lung parenchymal recoil and airway mucosal folding. Resident airway cells, as well as inflammatory cells, produce mediators, cytokines and growth factors that stimulate production of connective tissue proteins and proteoglycans that cause airway remodelling and altered mechanical function. Thickening of the airway wall internal to the smooth muscle layer can amplify the effect of smooth muscle shortening on airway calibre, and it could also stiffen the airway making it less distensible. Thickening of the airway wall external to the muscle can uncouple the airway from the distending force applied by the lung parenchyma. Early and aggressive anti-inflammatory medication may alter the natural history of asthma by preventing the structural changes that are a consequence of chronic allergic inflammation.

Biochemical markers, extracellular components in liver fibrosis and cirrhosis

Liver fibrosis and cirrhosis are common sequelae to diverse liver injuries in the tropics or Nigeria. The development of hepatic fibrosis or cirrhosis is due to increased synthesis, deposition, and possibly reduced degradation of hepatic extracellular matrix components, especially collagens, such as interstitial type I and III, basement membrane type IV, microfibrillar type VI, and pericellular type V, non-collagenous proteins, such as laminin, fibronectin, undulin, etc., and various types of proteoglycans, such as hyaluronan, etc. In Nigeria, the common approach for diagnosing or assessing the activity of connective tissue in this organ is the histological examination of a biopsy, if one is performed by a specialist physician. The liver biopsy provides a static picture of the changes that have already taken place in the liver. Another possible method is (where the facilities are available) a quantitative assessment of the liver biopsy by biochemical determination of total collagen via hydroxyproline. Biopsy is an invasive method and cannot be repeated often enough in the bid to ensuring an intensive follow-up of the changes taking place during the course of antifibrotic treatment or therapy. Thus, serum or other biological fluid assays for connective tissue proteins, such as the aminoterminal propeptide of type III Procollagen PIIINP, or the dimeric carboxyterminal domain of type IV collagen known as NCl or PIVCP, laminin, and others are essentially non-invasive and can be carried out repeatedly. In addition, the measurement of certain enzymes of connective tissue proteins in serum may the reflect activity of liver fibrogenesis. They offer the potential for diagnosis and therapeutic control. However, it is very important to note that circulating biochemical markers of fibrogenesis, fibrolysis or both may not reflect hepatic fibrosis or cirrhosis, since they are not liver-specific. Thus, the best diagnostic approach would be the identification and measurement in serum of the driving force of fibrogenic process.

Contractile and connective tissue protein content of human skeletal muscle: effects of 35 and 90 days of simulated microgravity and exercise countermeasures

We examined the effects of 35 and 90 days of simulated microgravity with or without resistance-exercise (RE) countermeasures on the content of the general skeletal muscle protein fractions (mixed, sarcoplasmic, and myofibrillar) and specific proteins that are critical for muscle function (myosin, actin, and collagen). Subjects from two studies, using either unilateral lower limb suspension (ULLS) or bed rest (BR), comprised four separate groups: 35 days ULLS (n =11), 35 days ULLS+RE (n = 10), 90 days BR (n = 9), and 90 days BR+RE (n = 8). RE consisted of four sets of seven maximal concentric and eccentric repetitions of the quadriceps femoris muscles that were performed 2 or 3 times per week. Pre- and post-simulated weightlessness muscle biopsies were analyzed from the vastus lateralis of all groups and the soleus of the 35-day ULLS and 90-day BR groups. The general protein fractions and the specific proteins myosin, actin, and collagen of the vastus lateralis were unchanged (P > 0.05) in both control and countermeasures groups over 35 and 90 days, despite large changes in quadriceps femoris muscle volume (35 days ULLS: -9%, 35 days ULLS+RE: +8%; and 90 days BR: -18%, 90 days BR+RE: -1%). The soleus demonstrated a decrease in mixed (35 days ULLS: -12%, P = 0.0001; 90 days BR: -12%, P = 0.004) and myofibrillar (35 days ULLS: -12%, P = 0.009; 90 days BR: -8%, P = 0.04) protein, along with large changes in triceps surae muscle volume (35 days ULLS: -11%; 90 days BR: -29%). Despite the loss of quadriceps femoris muscle volume or preservation with RE countermeasures during simulated microgravity, the quadriceps femoris muscles are able to maintain the concentrations of the general protein pools and the main contractile and connective tissue elements. Soleus muscle protein composition appears to be disproportionately altered during long-duration simulated weightlessness.

Serial analysis of gene expression (SAGE) in rat liver regeneration

We have applied serial analysis of gene expression for studying the molecular mechanism of the rat liver regeneration in the model of 70% partial hepatectomy. We generated three SAGE libraries from a normal control liver (NL library: 52,343 tags), from a sham control operated liver (Sham library: 51,028 tags), and from a regenerating liver (PH library: 53,061 tags). By SAGE bioinformatics analysis we identified 40 induced genes and 20 repressed genes during the liver regeneration. We verified temporal expression of such genes by real time PCR during the regeneration process and we characterized 13 induced genes and 3 repressed genes. We found connective tissue growth factor transcript and protein induced very early at 4 h after PH operation before hepatocytes proliferation is triggered. Our study suggests CTGF as a growth factor signaling mediator that could be involved directly in the mechanism of liver regeneration induction.

Differential expression of genes involved with apoptosis, cell cycle, connective tissue proteins, fuel substrate utilization, inflammation and mitochondrial biogenesis in copper-deficient rat hearts: implication of a role for Nfκb1

We hypothesized that the increase in mitochondrial proliferation in hearts from copper-deficient rats is due to an increase in expression of the transcriptional factor peroxisomal-like proliferating related coactivator 1α (Ppargc1a), which regulates transcriptional activity for many of the genes that encode for mitochondrial proteins. In addition to several transcriptional factors implicated in mitochondrial biogenesis, we also looked at a number of genes involved in cell cycle regulation and fuel substrate utilization. Long–Evans rats were placed on either a copper-adequate ( n=4) or copper-deficient ( n=4) diet 3 days post weaning and remained on the diet for 5 weeks; their copper deficiency status was confirmed using previously established assays. Custom oligo arrays spotted with genes pertinent to mitochondrial biogenesis were hybridized with cRNA probes synthesized from the collected heart tissue. Chemiluminescent array images from both groups were analyzed for gene spot intensities and differential gene expression. Our results did not demonstrate any significant increase in Ppargc1a or its implicated targets, as we had predicted. However, consistent with previous data, an up-regulation of genes that encode for collagen type 3, fibronectin and elastin were found. Interestingly, there was also a significant increase in the expression of the transcriptional factor nuclear factor κB1 (Nfκb1) in the copper-deficient treatment animals, compared to the control group, and this was confirmed by real time quantitative polymerase chain reaction. The results of this study merit the further investigation of the role of reactive oxidative species with regard to Nfκb1 in the copper deficient rat heart.

Preparation of collagen/poly(L-lactic acid) composite material for

Collagen is the major structural protein of connective tissues. It can be used as a prosthetic biomaterial applicable to artificial skin, tendon, ligaments, and collagen implants. The objective of this study is to investigate the possibility of realizing wound dressing medical products by the synthesis of composite materials with collagen and a biodegradable polymer, PLLA, via a surface modification process. Type I collagen was obtained from pig skin by a separation process. The structural characteristics of the extracted collagen were confirmed by SDS-polyacrylamide (PAcr) gel electrophoresis (PAGE) and FTIR. Also, PLLA-g-PAcr was synthesized by the radical polymerization of acrylamide initiated by AIBN in the presence of PLLA. The surface of PLLA was modified by the presence of the acrylamide residues. The structural characteristics of the copolymer were analyzed by FTIR,1H-NMR and contact angle measurements. The water uptake and WVTR of the collagen/PLLA-g-PAcr composite tended to increase with increasing collagen concentration and with decreasing EDC concentration.