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Spinal cord injury results in disruption of the cord microstructure, which is followed by inflammation leading to additional deterioration. Perivascular basement membranes are a component of the spinal cord microstructure that lies between blood vessels and astrocytes. The impact of disrupting the basement membrane structure on the expansion of inflammation has not been fully examined. The objective of this study was to clarify the relationship between damage to basement membranes and inflammation after spinal cord injury. Immunohistochemical analyses of the perivascular extracellular matrix were performed in a mouse spinal cord injury model. In normal tissue, the perivascular basement membrane was a single-layer structure produced by both endothelial cells and surrounding astrocytes. After spinal cord injury, however, the perivascular basement membrane often separated into an inner endothelial basement membrane and an outer parenchymal basement membrane. The altered basement membranes formed during the acute phase (within 7 days after spinal cord injury). During the subacute phase of injury, numerous monocytes and macrophages accumulated in the space between the separated basement membranes and infiltrated into the parenchyma where astrocytic endfeet were displaced. Infiltration of inflammatory cells from the injury core was attenuated coincident with the appearance of the glia limitans and glial scar. Furthermore, the outer parenchymal basement membrane was connected to the basement membrane of the glia limitans surrounding the injury core. Our data suggest that structurally altered basement membranes facilitate expansion of secondary inflammation during the subacute phase of spinal cord injury.

Intensive management of diabetic control at a stringent mean on-study PPG < 10.0 mmol/L will improve the life expectancy in diabetic dialysis patients. However, no range of HbA1c values obtained in this study showed any clear difference in clinical outcomes.

ABSTRACT. Effects of the collagen oligopeptide (COP) were examined by its repeat injection into the inflammatory rabbit Achilles tendon (Tendo calcaneus communis), in which tenositis was induced by injection of bacterial collagenase. COP was evaluated 5 times over a period of 3 weeks to 1 month after injection of collagenase. At 1 month after treatment, the therapeutic effect of COP was evaluated by examining the structure of collagen fibrils, amount and components of glycosaminoglycans (GAGs) and matrix metalloproteinases (MMPs), and compared with the saline injection, control, and normal groups. The Achilles tendon of rabbit in the control group (no COP injection) and saline injection group showed a notable increase in the number of fine collagen fibrils, a change in GAG composition and increase in the amount of pro-MMP-2, indicating the weakening of the tendon. In contrast, the size distribution of collagen fibrils, GAG composition and the amount of pro-MMP-2 was similar to those in the normal group. These results suggest that COP injection promotes healing processes of the tendon injury. KEY WORDS: collagen fibril, collagen oligopeptide, electron microscopy, glycosaminoglycans, rabbit tendon.J. Vet. Med. Sci. 70(12): 1295-1300, 2008 The basic function of a tendon is to convey the force exerted by a muscle to the bone. The mechanical load is not transmitted directly to the bone because tendon is a highly flexible connective tissue. This connective tissue is composed of two components: tendon cells and extracellular matrix (ECM) that consists of collagen and proteoglycans [1,21]. Collagen in a tendon is composed of mainly type I collagen and is arranged into bundles of collagen fibrils that are further organized into tendon fascicles [22]. Proteoglycan has its core protein covalently bound to glycosaminoglycan (GAG). GAG is a non-branched polysaccharide consisting of repeated units of amino acids and uronic acids. GAGs in ECM exist as proteoglycans except for hyaluronic acid (HA) that exists as a free GAG. Proteoglycans are classified into chondroitin sulphate (CS), dermatan sulphate (DS), heparan sulphate (HS), heparin or keratan sulphate according to their uronic acid subunit [3]. Decorin is the most abundant DS proteoglycan in tendon, and is reportedly involved in both the formation of collagen fibrils and adjustment of collagen fibril diameter [37]. However, its role in the turnover of tendon ECM has not yet been elucidated [16].Matrix metalloproteinase (MMP) is an enzyme that has zinc ion in its active core and requires calcium ion for maintenance of the activity. More than 20 types of MMP have been reported so far, and they play an important role in the turnover of tendon ECM [7,34]. MMPs are divided into the following types: collagenase (MMP-1, -8, -13), gelatinase (MMP-2, -9), stromelysin (MMP-3, -10), membrane , and others (including MMP-7, -11, -12) according to their biochemical properties [4]. However, how these MMPs are involved in the turnover of tendon ECM remains unclear.Inflammation of a tendo...