scholarly journals Biological Aspect of Pathophysiology for Frozen Shoulder

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Chul-Hyun Cho ◽  
Kwang-Soon Song ◽  
Beom-Soo Kim ◽  
Du Hwan Kim ◽  
Yun-Mee Lho
Keyword(s):  
Growth Factors ◽  
Matrix Metalloproteinases ◽  
Immune Cells ◽  
Frozen Shoulder ◽  
Matrix Remodeling ◽  
Biological Aspect ◽  
Novel Treatment ◽  
The Matrix ◽  
Basic Studies

It is fairly well understood that frozen shoulder involves several stages, which reflect the series of process from capsular inflammation and fibrosis to spontaneous resolution of this fibrosis. However, the underlying pathophysiologic process remains poorly determined. For this reason, management of frozen shoulder remains controversial. Determining the pathophysiological processes of frozen shoulder is a pivotal milestone in the development of novel treatment for patients with frozen shoulder. This article reviews what is known to date about the biological pathophysiology of frozen shoulder. Although articles for the pathophysiology of frozen shoulder provide inconsistent and inconclusive results, they have suggested both inflammation and fibrosis mediated by cytokines, growth factors, matrix metalloproteinases, and immune cells. Proinflammatory cytokines and growth factors released from immune cells control the action of fibroblast and matrix remodeling is regulated by the matrix metalloproteinases and their inhibitors. To improve our understanding of the disease continuum, better characterizing the biology of these processes at clearly defined stages will be needed. Further basic studies that use standardized protocols are required to more narrowly identify the role of cytokines, growth factors, matrix metalloproteinases, and immune cells. The results of these studies will provide needed clarity into the control mechanism of the pathogenesis of frozen shoulder and help identify new therapeutic targets for its treatment.

Matrix Metalloproteinases: Biologic Activity and Clinical Implications

2000 ◽  
Vol 18 (5) ◽  
pp. 1135-1135 ◽  
Author(s):  
Amy R. Nelson ◽  
Barbara Fingleton ◽  
Mace L. Rothenberg ◽  
Lynn M. Matrisian
Keyword(s):  
Matrix Metalloproteinases ◽  
Tumor Growth ◽  
Tumor Progression ◽  
Metastatic Tumor ◽  
The Body ◽  
Genetic Changes ◽  
Biologic Activity ◽  
The Matrix ◽  
Degradative Enzymes

ABSTRACT: Tumor progression is a complex, multistage process by which a normal cell undergoes genetic changes that result in phenotypic alterations and the acquisition of the ability to spread and colonize distant sites in the body. Although many factors regulate malignant tumor growth and spread, interactions between a tumor and its surrounding microenvironment result in the production of important protein products that are crucial to each step of tumor progression. The matrix metalloproteinases (MMPs) are a family of degradative enzymes with clear links to malignancy. These enzymes are associated with tumor cell invasion of the basement membrane and stroma, blood vessel penetration, and metastasis. They have more recently been implicated in primary and metastatic tumor growth and angiogenesis, and they may even have a role in tumor promotion. This review outlines our current understanding of the MMP family, including the association of particular MMPs with malignant phenotypes and the role of MMPs in specific steps of the metastatic cascade. As scientific understanding of the MMPs has advanced, therapeutic strategies that capitalize on blocking the enzymes have rapidly developed. The preclinical and clinical evolution of the synthetic MMP inhibitors (MMPIs) is also examined, with the discussion encompassing important methodologic issues associated with determining clinical efficacy of MMPIs and other novel therapeutic agents.

scholarly journals Role of bioactive molecules and maternal immune cells in breast-milk in type 2 diabetes mellitus risk reduction

2019 ◽  
Vol 12 (2) ◽  
pp. 69-79
Author(s):  
Tajudeen Yahaya ◽  
Mutiu Sifau
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Growth Factors ◽  
Breast Milk ◽  
Risk Reduction ◽  
Immune Cells ◽  
Bioactive Molecules

Inadequate breastfeeding or its total neglect has been mentioned in several studies as a contributing factor to the globally rising incidence of Type 2 diabetes mellitus (T2DM). However, the anti-diabetic role of breast-milk has not been given much attention. As such, this study was initiated to review and bring to update on the role of breastfeeding in the risk reduction of T2DM. Relevant information on the topic was retrieved from the reliable science databases, including PubMed, MedLine, Google Scholar, Researchgate, etc. The results showed that breast-milk is not energy dense and contains several health-enhancing bioactive molecules, including adipokines, antimicrobial and growth factors, cytokines, nutrients, and immune cells. Adipokines interact with the central nervous system to modulate certain physiological processes involved in energy balance, thereby programming an infant to be at a reduced risk for overweight, obesity and T2DM later in life. The antimicrobial and growth factors, as well as immune cells and bioactive nutrients may stimulate the growth of beneficial bacteria and/or inhibit the growth of pathogens. Thus, strengthen neonate defense mechanisms to effectively prevent infections as well as short and long-term disorders such as obesity and T2DM. In conclusion, nursing mothers are advised to breastfeed babies adequately before introducing them to complementary foods. To cater to the need of babies who may not have access to breastfeeding, healthcare providers should formulate infant formula using breast-milk components as basic constituents.

Molecular regulation of cellular invasion— role of gelatinase A and TIMP-2

1996 ◽  
Vol 74 (6) ◽  
pp. 823-831 ◽  
Author(s):  
Anita E. Yu ◽  
Robert E. Hewitt ◽  
David E. Kleiner ◽  
William G. Stetler-Stevenson
Keyword(s):  
Extracellular Matrix ◽  
Matrix Metalloproteinases ◽  
Tissue Inhibitors Of Metalloproteinases ◽  
Gelatinase A ◽  
Cellular Mechanisms ◽  
Cell Matrix ◽  
Matrix Interactions ◽  
The Matrix ◽  
Cell Matrix Interactions

Extracellular matrix (ECM) turnover is an event that is tightly regulated. Much of the coordinate (physiological) or discoordinate (pathological) degradation of the ECM is catalyzed by a class of proteases known as the matrix metalloproteinases (MMPs) or matrixins. Matrixins are a family of homologous Zn atom dependent endopeptidases that are usually secreted from cells as inactive zymogens. Net degradative activity in the extracellular environment is regulated by specific activators and inhibitors. One member of the matrixin family, gelatinase A, is regulated differently from other MMPs, suggesting that it may play a unique role in cell–matrix interactions, including cell invasion. The conversion from the 72 kDa progelatinase A to the active 62 kDa species may be a key event in the acquisition of invasive potential. This discussion reviews some recent findings on the cellular mechanisms involved in progelatinase A activation and, in particular, the role of tissue inhibitor of matrix metalloproteinases-2 (TIMP-2) and transmembrane containing metalloproteinases (MT-MMP) in this process.Key words: tissue inhibitors of metalloproteinases, metalloproteinase, gelatinases, extracellular matrix, activation.

scholarly journals Role of matrix metalloproteinase in the aneurismatic aortic disease

2004 ◽  
Vol 62 (3) ◽  
Author(s):  
Nicola Troisi ◽  
Alfredo Mazza ◽  
Felice Mazza ◽  
Gabriele Iannelli
Keyword(s):  
Matrix Metalloproteinases ◽  
Aortic Disease ◽  
Endothelial Damage ◽  
Matrix Proteins ◽  
Tissue Destruction ◽  
The Matrix ◽  
Drug Inhibition ◽  
Atherosclerotic Aneurysm ◽  
Aneurysm Diameter

The aorta is involved in a large variety of diseases and the atherosclerotic aneurysms represent the most common type of these. Recent reports have attempted to clarify the mechanisms, that cause the formation and the progression of the atherosclerotic aneurysms, caused not only by the atherosclerosis. One of the features of this disease is the extensive proteolytic destruction of structural matrix proteins in the aortic wall realized by the matrix metalloproteinases. The atherosclerotic aneurysm can be considered a disease caused by an imbalance between connective tissue destruction and its repair. Knowledge of the role played by matrix metalloproteinases in the formation process of the aneurysms has made the inhibition of these proteins a logical therapeutic strategy. Once completed the aneurysm treatment, surgical or endovascular, the endothelial damage must disappear; the persistence of this damage, after endovascular procedure, is the cause of the formation of the endoleaks. The preoperative matrix metalloproteinases plasmatic levels are related to the aneurysm diameter and after endovascular treatment these values come back normal, except in the case of presence of an endoleak, that don’t make possible the reduction of these values. In spite of that, obscure points still remain, above all about the dosage of these proteins and their inhibition through drugs with clear metalloproteinases- inhibiting properties. The aim of this study is to clarify further on the mechanisms of the formation of the aneurysms with particular care to the matrix metalloproteinases, their dosage and their drug inhibition.

scholarly journals The Role of Tumor-Associated Macrophages in Colorectal Carcinoma Progression

2018 ◽  
Vol 45 (1) ◽  
pp. 356-365 ◽  
Author(s):  
Xiaoming Zhong ◽  
Bin Chen ◽  
Zhiwen Yang
Keyword(s):  
Extracellular Matrix ◽  
Tumor Microenvironment ◽  
Colorectal Carcinoma ◽  
Tumor Growth ◽  
Immune Cells ◽  
Strong Evidence ◽  
Extracellular Matrix Remodeling ◽  
Matrix Remodeling ◽  
Tumor Associated Macrophages

Tumor-associated macrophages (TAMs) are one of the most abundant immune cells in the tumor microenvironment, and they play a pivotal role in prompting the various tumor growth. However, the role of TAMs in colorectal carcinoma (CRC) is controversial, because a few papers report that TAMs is beneficial to CRC patients. In this review, we discuss the good or bad roles of TAMs in CRC progression. Interestingly, recent studies provide strong evidence that TAMs facilitate CRC growth, but do not exert tumor suppressive activities. TAMs can stimulate CRC growth by altering extracellular matrix remodeling, tumor metabolism, angiogenesis, as well as the tumor microenvironment. Therefore, TAMs could serve as a target for CRC therapeutic treatment.

scholarly journals Growth Factors, Their Receptors, Neuropeptide-Containing Innervation, and Matrix Metalloproteinases in the Proximal and Distal Ends of the Esophagus in Children With Esophageal Atresia

Medicina ◽  
2011 ◽  
Vol 47 (8) ◽  
pp. 453 ◽  
Author(s):  
Māra Pilmane ◽  
Linda Ozoliņa ◽  
Zane Ābola ◽  
Aigars Pētersons ◽  
Vjačeslavs Popkovs ◽  
...  
Keyword(s):  
Growth Factors ◽  
Matrix Metalloproteinases ◽  
Esophageal Atresia ◽  
Proximal Part ◽  
Histopathological Study ◽  
Pgp 9.5 ◽  
Proximal Esophagus ◽  
Proliferation And Differentiation ◽  
High Incidence

Objective. The pathogenesis of esophageal atresia (EA) remains unknown despite a relatively high incidence of this anomaly in population affecting 1 newborn per 3000 live births. The aim of this study was to examine the relative occurrence of growth factors, their receptors, neuropeptide- containing innervation, and tissue-degradating enzymes – matrix metalloproteinases – in the proximal and distal parts of the esophagus with EA. Materials and Methods. A histopathological study was conducted on 15 patients with EA. Tissues were processed for NGFRp75, PGP 9.5, TGF-β, FGFR, VEGF, EGFR and MMP-2 by means of biotin-streptavidin immunohistochemistry. Results. In the control and EA-affected distal esophageal specimens, numerous and abundant NGFR-containing structures were detected, while in the proximal part of the esophagus, a decrease in their number was observed in patients. PGP 9.5 also marked neuronal structures similarly. TGF-β was found only in occasional cells in the EA-affected esophageal specimens, while control material demonstrated moderate to numerous TGF-β-containing structures. Abundance of FGFR and only occasional appearance of VEGF-positive cells were found in both the control and EA-affected material. A moderate number of connective tissue cells in controls contained EGFR. Compared with controls, the number of MMP-2 expressing cells in the EA-affected tissues was decreased in the proximal esophagus. Conclusions. A decrease in PGP 9.5-containing neuronal structures in the proximal esophagus supports insufficient innervation of this part of the organ in EA. A decrease in MMP-2 positive cells in the esophageal atresia-affected proximal esophagus indicates also a possible decrease of tissue adaptive and regenerative reactions. Low expression of TGF-β and almost the absence of EGFR in the EA-affected specimens may result in disturbances of cell growth, proliferation, and differentiation, indicating a significant role of these substances in morphopathogenesis of EA. FGFR and VEGF seem not to characterize EA pathogenesis.

scholarly journals Role of subnetworks mediated by $$\hbox {TNF}\alpha$$, IL-23/IL-17 and IL-15 in a network involved in the pathogenesis of psoriasis

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Rakesh Pandey ◽  
Yusur Al-Nuaimi ◽  
Rajiv Kumar Mishra ◽  
Sarah K. Spurgeon ◽  
Marc Goodfellow
Keyword(s):  
Complex Network ◽  
Immune Cells ◽  
Immune Cell ◽  
Treatment Strategies ◽  
Tnf Alpha ◽  
Cell Network ◽  
Novel Treatment ◽  
Future Drug ◽  
Novel Treatment Strategies

AbstractPsoriasis is a chronic inflammatory skin disease clinically characterized by the appearance of red colored, well-demarcated plaques with thickened skin and with silvery scales. Recent studies have established the involvement of a complex signalling network of interactions between cytokines, immune cells and skin cells called keratinocytes. Keratinocytes form the cells of the outermost layer of the skin (epidermis). Visible plaques in psoriasis are developed due to the fast proliferation and unusual differentiation of keratinocyte cells. Despite that, the exact mechanism of the appearance of these plaques in the cytokine-immune cell network is not clear. A mathematical model embodying interactions between key immune cells believed to be involved in psoriasis, keratinocytes and relevant cytokines has been developed. The complex network formed of these interactions poses several challenges. Here, we choose to study subnetworks of this complex network and initially focus on interactions involving $$\hbox {TNF}_{\alpha }$$ TNF α , IL-23/IL-17, and IL-15. These are chosen based on known evidence of their therapeutic efficacy. In addition, we explore the role of IL-15 in the pathogenesis of psoriasis and its potential as a future drug target for a novel treatment option. We perform steady state analyses for these subnetworks and demonstrate that the interactions between cells, driven by cytokines could cause the emergence of a psoriasis state (hyper-proliferation of keratinocytes) when levels of $$\hbox {TNF}_{\alpha }$$ TNF α , IL-23/IL-17 or IL-15 are increased. The model results explain and support the clinical potentiality of anti-cytokine treatments. Interestingly, our results suggest different dynamic scenarios underpin the pathogenesis of psoriasis, depending upon the dominant cytokines of subnetworks. We observed that the increase in the level of IL-23/IL-17 and IL-15 could lead to psoriasis via a bistable route, whereas an increase in the level of $$\hbox {TNF}_{\alpha }$$ TNF α would lead to a monotonic and gradual disease progression. Further, we demonstrate how this insight, bistability, could be exploited to improve the current therapies and develop novel treatment strategies for psoriasis.

Pathogenesis of pterygia: role of cytokines, growth factors, and matrix metalloproteinases

2004 ◽  
Vol 23 (2) ◽  
pp. 195-228 ◽  
Author(s):  
Nick Di Girolamo ◽  
Jeanie Chui ◽  
Minas T Coroneo ◽  
Denis Wakefield
Keyword(s):  
Growth Factors ◽  
Matrix Metalloproteinases
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