scholarly journals Hyaluronic Acid Treatment Improves Healing of the Tenorrhaphy Site by Suppressing Adhesions through Extracellular Matrix Remodeling in a Rat Model

Polymers ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 928
Author(s):  
Kwang Hyeon Ahn ◽  
Eun Soo Park ◽  
Chang Yong Choi ◽  
Han Gyu Cha ◽  
Yongsung Hwang ◽  
...  
Keyword(s):  
Hyaluronic Acid ◽  
Transforming Growth Factor ◽  
Adhesion Formation ◽  
Plasminogen Activator Inhibitor ◽  
Inflammatory Cells ◽  
Collagen Type I ◽  
Control Group ◽  
Type I ◽  
Matrix Remodeling ◽  
Plasminogen Activator Inhibitor 1

Due to the limited supply of vessels and nerves, acute or chronic tendon injuries often result in significant and persistent complications, such as pain and sprains, as well as the loss of joint functions. Among these complications, tendon adhesions within the surrounding soft tissue have been shown to significantly impair the range of motion. In this study, to elucidate the effects of a hyaluronic acid (HA) injection at the site of tenorrhaphy on tendon adhesion formation, we used a full transection model of a rat’s Achilles tendon to investigate the anti-adhesive function of HA. Our initial findings showed that significantly lower adhesion scores were observed in the HA-treated experimental group than in the normal saline-treated control group, as determined by macroscopic and histological evaluations. Hematoxylin and eosin, as well as picrosirius red staining, showed denser and irregular collagen fibers, with the larger number of infiltrating inflammatory cells in the control group indicating severe adhesion formation. Furthermore, we observed that the expression of tendon adhesion markers in operated tendon tissue, such as collagen type I, transforming growth factor-β1, and plasminogen activator inhibitor-1, was suppressed at both the gene and protein levels following HA treatment. These results suggest that HA injections could reduce tendon adhesion formation by significantly ameliorating inflammatory-associated reactions.

scholarly journals Therapeutic Effects of Acupuncture through Enhancement of Functional Angiogenesis and Granulogenesis in Rat Wound Healing

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Sang In Park ◽  
Yun-Young Sunwoo ◽  
Yu Jin Jung ◽  
Woo Chul Chang ◽  
Moon-Seo Park ◽  
...  
Keyword(s):  
Wound Healing ◽  
Collagen Type ◽  
Interleukin 1 ◽  
Treated Group ◽  
Collagen Type I ◽  
Control Group ◽  
Therapeutic Effects ◽  
Type I ◽  
Matrix Remodeling ◽  
Cd 31

Acupuncture regulates inflammation process and growth factors by increasing blood circulation in affected areas. In this study, we examined whether acupuncture has an effect on wound healing in injured rat. Rats were assigned randomly into two groups: control group and acupuncture group. Acupuncture treatment was carried out at 8 sites around the wounded area. We analyzed the wound area, inflammatory cytokines, proliferation of resident cells, and angiogenesis and induction of extracelluar matrix remodeling. At 7 days after-wounding the wound size in acupuncture-treat group was decreased more significantly compared to control group. In addition, the protein levels of proinflammatory cytokines such as tumor necrosis factor-α(TNF-α) and interleukin-1β(IL-1β) were significantly decreased compared to the control at 2 and 7 days post-wounding. Also, we analyzed newly generated cells by performing immunostaining for PCNA and using several phenotype markers such as CD-31,α-SMA, and collagen type I. In acupuncture-treated group, PCNA-positive cell was increased and PCNA labeled CD-31-positive vessels,α-SMA- and collagen type I-positive fibroblastic cells, were increased compared to the control group at 7 days post-wounding. These results suggest that acupuncture may improve wound healing through decreasing pro-inflammatory response, increasing cell proliferation and angiogenesis, and inducing extracellular matrix remodeling.

PAI-1 gene 4G/5G polymorphism, cytokine levels and their relations with metabolic parameters in obese children

2008 ◽  
Vol 99 (02) ◽  
pp. 352-356 ◽  
Author(s):  
Muammer Yuce ◽  
Ayse Yazici ◽  
Hasibe Verdi ◽  
F. Belgin Ataç ◽  
Sibel Kinik ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Plasminogen Activator Inhibitor ◽  
Control Group ◽  
Model Assessment ◽  
Obese Children ◽  
Plasminogen Activator Inhibitor 1 ◽  
Necrosis Factor Alpha ◽  
Pai 1

SummaryObesity is associated with the changes of plasminogen activator inhibitor-1 (PAI-1), tumor necrosis factor-alpha (TNFα) and transforming growth factor beta (TGFβ) levels. However, the precise effect of the 4G allele on obesity is still contradictory. Here, we aimed to elucidate the role of the 4G/5G polymorphism of the PAI-1 gene on the PAI-1 level and determine the associations between cytokines, glucose and lipid metabolism parameters in obese children. Thirty-nine obese children (mean age 11.4 ± 3.3 years) and 38 age-matched healthy control group (mean age 10.3 ± 3.5 years) were included in the study. In all cases, serum levels of glucose, lipid and insulin were measured, homeostasis model assessment of insulin resistance (HOMAIR) was calculated, and 4G/5G polymorphism of PAI-1 gene, plasma PAI-1 level and serum TNFα and TGFβ levels were studied. The mean relative body mass index (BMI) and HOMA-IR score, VLDL,TG, insulin, PAI-1,TNFα levels were higher, and HDL and TGFβ levels were lower in the obese group. The frequency of the 4G/4G genotype was considerably higher in obese children than in controls. Also, a positive correlation was found between PAI-1 and TNFα levels, and relative BMI, HOMA-IR score, insulin,TG, HDL levels. TGFβ was inversely correlated only with relative BMI. There was no correlation among three cytokines. In conclusion, childhood obesity contributes to higher PAI-1 andTNFα and lowerTGFβ levels. Especially PAI-1 andTNFα accompany insulin resistance and dyslipidemia.

scholarly journals Plasminogen activator inhibitor-1 (PAI-1) is cardioprotective in mice by maintaining microvascular integrity and cardiac architecture

Blood ◽  
2010 ◽  
Vol 115 (10) ◽  
pp. 2038-2047 ◽  
Author(s):  
Zhi Xu ◽  
Francis J. Castellino ◽  
Victoria A. Ploplis
Keyword(s):  
Plasminogen Activator ◽  
Cardiac Fibrosis ◽  
Transforming Growth Factor ◽  
Plasminogen Activator Inhibitor ◽  
Transforming Growth Factor Β ◽  
Heart Tissue ◽  
Matrix Remodeling ◽  
Plasminogen Activator Inhibitor 1 ◽  
Activator Inhibitor ◽  
Pai 1

Abstract Although the involvement of plasminogen activator inhibitor-1 (PAI-1) in fibrotic diseases is well documented, its role in cardiac fibrosis remains controversial. The goal of this study was to determine the effect of a PAI-1 deficiency (PAI-1−/−) on the spontaneous development of cardiac fibrosis. PAI-1−/− mice developed pervasive cardiac fibrosis spontaneously with aging, and these mice displayed progressively distorted cardiac architecture and markedly reduced cardiac function. To mechanistically elucidate the role of PAI-1 in cardiac fibrosis, 12-week-old mice were chosen to study the biologic events leading to fibrosis. Although fibrosis was not observed at this early age, PAI-1−/− hearts presented with enhanced inflammation, along with increased microvascular permeability and hemorrhage. A potent fibrogenic cytokine, transforming growth factor-β (TGF-β), was markedly enhanced in PAI-1−/− heart tissue. Furthermore, the expression levels of several relevant proteases associated with tissue remodeling were significantly enhanced in PAI-1−/− hearts. These results suggest that PAI-1 is cardioprotective, and functions in maintaining normal microvasculature integrity. Microvascular leakage in PAI-1−/− hearts may provoke inflammation, and predispose these mice to cardiac fibrosis. Therefore, a PAI-1 deficiency contributes to the development of cardiac fibrosis by increasing vascular permeability, exacerbating local inflammation, and increasing extracellular matrix remodeling, an environment conducive to accelerated fibrosis.

Biocompatibility study of modified injectable hyaluronic acid hydrogel with mannitol/BSA to alveolar bone cells

2020 ◽  
pp. 088532822097174
Author(s):  
Kwanhatai Areevijit ◽  
Nirada Dhanesuan ◽  
Jittima Amie Luckanagul ◽  
Sorasun Rungsiyanont
Keyword(s):  
Alkaline Phosphatase ◽  
Hyaluronic Acid ◽  
Collagen Type ◽  
Alveolar Bone ◽  
Bone Cells ◽  
Collagen Type I ◽  
Control Group ◽  
Type I ◽  
Hyaluronic Acid Hydrogel ◽  
Alveolar Bone Cells

The quality and quantity of bone are crucial to the success of dental implant treatment. Recently, bone grafting materials have reached some limitations. This study aimed to evaluate the biocompatibility of novel drug delivery material, injectable methacrylated hyaluronic acid hydrogel incorporated with different ratios of mannitol and BSA (Man/BSA MeHA), to human alveolar bone cells. The three-dimensionally encapsulated cell culture was evaluated with the resazurin cell viability test, alkaline phosphatase activity assay, immunohistochemistry test for collagen type-I synthesis, and cell morphology. The results showed that the encapsulated cells were viable in all four ratios of Man/BSA MeHA hydrogel and the average metabolic rate was not less than the control group. The morphology test showed round shape cells at the upper portion of the hydrogel and fibroblast-like or polygonal shape at the lower portion of hydrogel next to the culture plate. All four groups could express enzyme alkaline phosphatase and collagen type-I. In conclusion, four ratios of Man/BSA MeHA hydrogel were biocompatible with primary human alveolar bone cells.

scholarly journals Effectiveness of Hyaluronan Autocross-Linked-Based Gel in the Prevention of Peritendinous Adherence Following Tenolysis

2021 ◽  
Vol 11 (16) ◽  
pp. 7613
Author(s):  
Andrea Marchesini ◽  
Francesco De Francesco ◽  
Pier Paolo Pangrazi ◽  
Letizia Senesi ◽  
Andrea Campodonico ◽  
...  
Keyword(s):  
Gene Expression ◽  
Adhesion Formation ◽  
Rabbit Model ◽  
Treated Group ◽  
Collagen Type I ◽  
Biomechanical Analysis ◽  
Surgical Approaches ◽  
Control Group ◽  
Type I ◽  
Electron Microscopic

Peritendinous adhesions are a frequent occurrence following tenolysis and present a major clinical challenge regarding prevention and management, with no recovery assured from conservative or surgical approaches. Herein, we investigated the effectiveness of Hyaloglide®, a hyaluronan gel-based product with a novel autocross-linked technology, in a rabbit model affected by tenolysis on the flexor digitorum communis tendon (FDC). A 1.5-cm-long scrubbing of the tendon surface was performed bilaterally to induce peritendinous adhesion on FDC of 30 animals with subsequent application of Hyaloglide® on the surrounding injured area, in one randomly chosen tendon. The contralateral tendon was treated with saline solution as the control. We sacrificed the rabbit models after 45 days of surgery and quantitatively assessed the generation of peritendinous adherence and regeneration of the tendon sheaths using histological (hematossyline-eosine, masson’s trichromic), histomorphometrical (Tang score, Soslowsky Svesson, and Cook score), light electron microscopic, and gene expression investigations. Four rabbits were devoted to biomechanical analysis. Peritendinous adhesions were limited in Hyaloglide®-treated tendons; moreover, well-regenerated tendon sheaths were observed conversely to untreated tendons presenting with extensive areas of adhesions on the tendon surface. Histomorphometrical analysis revealed an adhesion score (Tang score) significantly better in the treated group (p = 0.001 *) compared to the control group. Moreover, the Soslowsky, Svensson, and Cook score parameters revealed a significantly improved regeneration for fiber structure, cellularity, and vascularity in the treated group (p = 0.001 *). No differences were reported for cartilaginous formation (p = 0.08). Gene expression analysis showed a significant increase in collagen type I expression in the treated group compared to the control group, while metalloprotease 1 and 9 were significantly increased in the control group. Biomechanical analysis did not show significant differences in both groups. Hyaloglide® treatment was safe and well-tolerated, generating improved tissue status. Local application of Hyaloglide® prevents adhesion formation after tenolysis and promotes normal healing with regeneration of the synovial sheath in a rabbit model.

Relationship of Plasminogen Activator Inhibitor-1 Levels following Thrombolytic Therapy with rt-PA as Compared to Streptokinase and Patency of Infarct Related Coronary Artery

1999 ◽  
Vol 82 (07) ◽  
pp. 104-108 ◽  
Author(s):  
Franck Paganelli ◽  
Marie Christine Alessi ◽  
Pierre Morange ◽  
Jean Michel Maixent ◽  
Samuel Lévy ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Thrombolytic Therapy ◽  
Plasminogen Activator ◽  
Plasminogen Activator Inhibitor ◽  
Control Group ◽  
Plasminogen Activator Inhibitor 1 ◽  
Vessel Patency ◽  
Activator Inhibitor ◽  
Pai 1

Summary Background: Type 1 plasminogen activator inhibitor (PAI-1) is considered to be risk factor for acute myocardial infarction (AMI). A rebound of circulating PAI-1 has been reported after rt-PA administration. We investigated the relationships between PAI-1 levels before and after thrombolytic therapy with streptokinase (SK) as compared to rt-PA and the patency of infarct-related arteries. Methods and Results: Fifty five consecutive patients with acute MI were randomized to strep-tokinase or rt-PA. The plasma PAI-1 levels were studied before and serially within 24 h after thrombolytic administration. Vessel patency was assessed by an angiogram at 5 ± 1days. The PAI-1 levels increased significantly with both rt-PA and SK as shown by the levels obtained from a control group of 10 patients treated with coronary angioplasty alone. However, the area under the PAI-1 curve was significantly higher with SK than with rt-PA (p <0.01) and the plasma PAI-1 levels peaked later with SK than with rt-PA (18 h versus 3 h respectively). Conversely to PAI-1 levels on admission, the PAI-1 levels after thrombolysis were related to vessel patency. Plasma PAI-1 levels 6 and 18 h after SK therapy and the area under the PAI-1 curve were significantly higher in patients with occluded arteries (p <0.002, p <0.04 and p <0.05 respectively).The same tendency was observed in the t-PA group without reaching significance. Conclusions: This study showed that the PAI-1 level increase is more pronounced after SK treatment than after t-PA treatment. There is a relationship between increased PAI-1 levels after thrombolytic therapy and poor patency. Therapeutic approaches aimed at quenching PAI-1 activity after thrombolysis might be of interest to improve the efficacy of thrombolytic therapy for acute myocardial infarction.

Elevated levels of activin A in clinical and experimental pulmonary hypertension

2009 ◽  
Vol 106 (4) ◽  
pp. 1356-1364 ◽  
Author(s):  
Arne Yndestad ◽  
Karl-Otto Larsen ◽  
Erik Øie ◽  
Thor Ueland ◽  
Camilla Smith ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Transforming Growth Factor ◽  
Experimental Studies ◽  
Plasminogen Activator Inhibitor ◽  
Muscle Cells ◽  
Activin A ◽  
Plasminogen Activator Inhibitor 1 ◽  
And Control

Activin A, a member of the transforming growth factor (TGF)-β superfamily, is involved in regulation of tissue remodeling and inflammation. Herein, we wanted to explore a role for activin A in pulmonary hypertension (PH). Circulating levels of activin A and its binding protein follistatin were measured in patients with PH ( n = 47) and control subjects ( n = 14). To investigate synthesis and localization of pulmonary activin A, we utilized an experimental model of hypoxia-induced PH. In mouse lungs, we also explored signaling pathways that can be activated by activin A, such as phosphorylation of Smads, which are mediators of TGF-β signaling. Possible pathophysiological mechanisms initiated by activin A were explored by exposing pulmonary arterial smooth muscle cells in culture to this cytokine. Elevated levels of activin A and follistatin were found in patients with PH, and activin A levels were significantly related to mortality. Immunohistochemistry of lung autopsies from PH patients and lungs with experimental PH localized activin A primarily to alveolar macrophages and bronchial epithelial cells. Mice with PH exhibited increased pulmonary levels of mRNA for activin A and follistatin in the lungs, and also elevated pulmonary levels of phosphorylated Smad2. Finally, we found that activin A increased proliferation and induced gene expression of endothelin-1 and plasminogen activator inhibitor-1 in pulmonary artery smooth muscle cells, mediators that could contribute to vascular remodeling. Our findings in both clinical and experimental studies suggest a role for activin A in the development of various types of PH.

scholarly journals Microinflammation Factors in the Common Diseases of the Heart and Kidneys

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Danijela Tasic ◽  
Sonja Radenkovic ◽  
Gordana Kocic ◽  
Marina Deljanin Ilic ◽  
Aleksandra Ignjatovic
Keyword(s):  
Kidney Diseases ◽  
Plasminogen Activator Inhibitor ◽  
Cardiorenal Syndrome ◽  
High Density Lipoproteins ◽  
Control Group ◽  
C Reactive Protein ◽  
Plasminogen Activator Inhibitor 1 ◽  
Reactive Protein ◽  
Lipid Status ◽  
Pai 1

Aim. To determine levels of interleukin-8 (IL-8) and plasminogen activator inhibitor-1 (PAI-1) in different cardiorenal syndrome (CRS) modalities and to compare findings to some already investigated direct and indirect parameters of inflammation and atherosclerosis.Materials and Methods. Testing involved 114 examinees, divided into control and clinical groups suffering from different modalities and were formed according to the basis of a valid classification for CRS.Results. C-reactive protein (CRP) was significantly higher in all CRSs in comparison to the control groupP<0.05. PAI-1 in CRSs was statistically higher than in the control group. IL-8 was increased in all CRSs, and especially in CRS-5, where no significance was found. PAI-1 correlated with IL-8 in all CRSs, with significant value in CRS-2 and CRS-5. Correlation for PAI-1 and high-density lipoproteins (HDL) was found in CRS-4, while IL-8 was found to be related to CRP level in all CRSs, with significance only in CRS-1P<0.001.Conclusions. C-reactive protein, IL-8, and PAI-1 could be useful for clinical differentiation of chronic modalities of CRSs. Inflammation was the most pronounced in CRS-4. Lipid status parameters could be useful for differentiation of CRSs. Furthermore, HDL in chronic primary kidney diseases and triglycerides and total cholesterol in CRS-5 could be valuable.

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