Expression of Matrix Metalloproteinase-2, Matrix Metalloproteinase-9, Tissue Inhibitor of Metalloproteinase-1, and Changes in Alveolar Septa in Patients with Chronic Obstructive Pulmonary Disease

Abstract

Background This study investigated the relationship between the pathological alteration of alveolar septa and (1) pulmonary function and (2) matrix metalloproteinase (MMP)-2, MMP-9, and tissue inhibitor matrix metalloproteinase 1 (TIMP-1) expression in chronic obstructive pulmonary disease (COPD). Material/Methods Sixty patients with pulmonary disease were divided into control (n=20) and COPD (n=40) groups. Postoperative lung tissue specimens were examined. Hematoxylin and eosin and elastin van Gieson staining detected pathological alterations of pulmonary alveolar septa. Septa thickness was measured. MMP-2, MMP-9, and TIMP-1 expression levels were detected by immunohistochemical staining. Correlations were determined by Pearson analysis. Results Forced expiratory volume in 1 s (FEV 1 ), forced vital capacity, FEV 1 percent predicted (FEV 1 %pre), and diffusion capacity of carbon monoxide percent predicted (DLCO%pre) in COPD patients were significantly lower than in those of the control group ( P <0.05). MMP-2, MMP-9, and TIMP-1 expression levels were significantly higher in the COPD group than in control, especially the severe group ( P <0.05). Septa thickness was negatively correlated with FEV 1 %pre ( r =−0.335; P <0.05) and positively correlated with MMP-2 and TIMP-1 expression ( P <0.05). Proportion of collagenous fiber was negatively correlated with FEV 1 %pre and DLCO%pre ( P <0.01), and positively correlated with MMP-2, MMP-9, and TIMP-1 expression ( P <0.01). Proportion of elastic fibers was negatively correlated with collagenous fiber. Conclusions The pathological alteration of alveolar septa was correlated with pulmonary function and expression levels of MMP-2, MMP-9, and TIMP-1, which can play vital roles in COPD progression.

Zanthoxylum bungeanum Seed Oil Attenuates LPS-Induced BEAS-2B Cell Activation and Inflammation by Inhibiting the TLR4/MyD88/NF-κB Signaling Pathway

“…When stimulated, COX-2 expression is rapidly upregulated, which can induce acute inflammatory response in humans and animals. MMP-2 and MMP-9 are considered to be important collagenases in inflammatory diseases, and the synthesis and secretion of MMP-2 and MMP-9 are highly related to TNF-α [43]. IL-10 expression can reduce lung neutrophil infiltration and inhibit the expression of TNF-α, IL-6, and MCP-1.…”

Glycyrrhizic Acid against Mycoplasma gallisepticum-Induced Inflammation and Apoptosis Through Suppressing the MAPK Pathway in Chickens

“…The GA and tiamulin treatment were both effective in inhibiting the expression of MG-activated p-ERK, p-JNK, p-p38, and p-jun (Figure ). Downstream MMPs of the MAPK pathway have been demonstrated to be involved in the emergence and progression of various lung diseases. , In chronic obstructive pulmonary disease, pathological changes in the alveolar septum correlate with lung function and MMP-2 and MMP-9 expression levels . Another study demonstrated that MMP2/9 is the predominant regulator of the cytotoxic effects induced by amyloid-β in lung cancer cells .…”

“…56,57 In chronic obstructive pulmonary disease, pathological changes in the alveolar septum correlate with lung function and MMP-2 and MMP-9 expression levels. 58 Another study demonstrated that MMP2/9 is the predominant regulator of the cytotoxic effects induced by amyloid-β in lung cancer cells. 59 We therefore also examined the expression of MMP2 and MMP9 associated with the lung injury in vivo and in vitro.…”

Clinical and molecular features of virus-induced acute exacerbations of chronic obstructive pulmonary diseas

“…Тройную Таблица 1. Основные характеристики пациентов, включенных в исследование 57 (95) 3 (5) 55 (91,7) 5 (8,3) 56 (93,3) 4 (6,7) 0 На момент индексного обострения ХОБЛ в плазме крови пациентов методом твердофазного иммуноферментного анализа определяли маркеры: ■ эозинофильного воспаления: эозинофильный катионный белок (ЕСР), IL-5 [16,23]; ■ нейтрофильного воспаления: нейтрофильная эластаза, гранулоцитарно-макрофагальный колониестимулирущий фактор (GM-CSF) [20,21]: ■ макрофагального воспаления: моноцитарный хемотаксический протеин 1 (МСР-1) [24]; ■ фиброзирования: фактор роста фибробластов 2 (FGF-2), трансформирующий фактор роста бета 1 (TGF-β1), гиалуроновая кислота, N-терминальный пептид проколлагена III типа (PIIINP) [25]; ■ а также уровень матриксных металлопротеиназ (ММР) 1 и 9 изоформ [26], IL-1β, С-реактивного белка (СРБ).…”