Serum markers of lamellar basement membrane degradation and lamellar histopathological changes in horses affected with laminitis

Abstract

Summary In order better to evaluate the extent to which degradation of the lamellar basement membrane (LBM) by matrix metalloproteinases (MMP) occurs in equine laminitis, we determined the concentration of type IV collagen and laminin in normal and laminitic horses, using specific immunoassays. Blood samples were obtained from both the jugular and the cephalic veins of horses (n = 10) before and after the induction of acute alimentary laminitis by carbohydrate overload. Jugular and cephalic venous blood samples were also obtained from horses affected with naturally occurring laminitis (n = 16) and nonlaminitic controls (n = 8). The serum collagen IV concentration was not changed following the induction of laminitis in the experimental group. Serum collagen IV concentration was increased in jugular venous blood obtained from cases of naturally occurring laminitis (mean ± s.e. 218.04 ± 18.59 ng/ml) compared with nonlaminitic controls (157.50 ± 10.93 ng/ml) (P<0.05). Serum collagen IV concentration was also increased in jugular venous blood obtained from severely laminitic horses (219.50 ± 18.18 ng/ml) compared with nonlaminitic controls (157.50 ± 10.93 ng/ml) (P<0.05). A difference in serum concentration of collagen IV was not identified based on chronicity of naturally occurring laminitis. Serum laminin concentration did not differ between laminitic and nonlaminitic horses. Differences in serum laminin concentration were not identified based on sampling location (jugular orcephalic vein), severity of laminitic pain, or chronicity of spontaneous laminitis. In conclusion, the circulating concentration of collagen IV was increased in horses affected with naturally occurring laminitis. The potential role for serum collagen IV assay for characterisation of equine laminitis warrants further investigation.

Ultrastructure Study of Transgenic Ren2 Rat Aorta – Part 1: Endothelium and Intima

“…These basal adhesion plaques were reminiscent of similar structures termed hemidesmosomes (cell-matrix attachments) that have been identified in laminitic ponies; therefore, the term hemidesmosome-like structures is appropriate. In laminitic ponies, the hemidesmosome structures act as adhesion plaques between the keratinocyte and the interstitial matrix (epithelial-matrix connections or adhesion plaques) and are reduced in number [30,31]. In the SDC and Ren2 vasculature, these structures act as basal adhesion plaques between the EC and the elastin lamina matrix of the IEL [32].…”

Neuropathic Pain Management in Chronic Laminitis

“…[5][6][7][8][9] Locally released and activated MMPs mediate degradation of the collagen components of the basement membrane (BM) that is interposed between the secondary dermal (SDL) and epidermal lamellae (SEL) and cause a separation of the SEL from the BM. 4,[10][11][12][13][14] Sensory innervation of the foot consists of thick myelinated A-fibers (largely A β ) transmitting low-threshold mechanical information and small thin myelinated (A δ -fibers) and un-myelinated afferents (C-fibers) which express a variety of peptides and transmit high-threshold nociceptive information. [15][16][17][18][19] The A β fibers innervate lamellated corpuscles (comparable with Pacinian corpuscles) clustered below the digital cushion in the heel segment of the hoof that function as proprioceptors and provide a secure gait.…”

Influência da heparina sódica na ocorrência de laminite eqüina induzida por sobrecarga de carboidratos

“…A complexidade da patogênese torna o tratamento difícil e oneroso e a doença freqüentemente evolui para um quadro grave e, às vezes, morte do animal. Vários são os fatores envolvidos no desenvolvimento de laminite, com destaque para as disfunções gastrintestinais, hipoperfusão periférica, endotoxemia e aumento sistêmico e local das concentrações de citocinas pró-inflamatórias, capazes de aumentar a atividade das metaloproteinases no tecido conectivo (Johnson et al, 2000). Esses eventos são acompanhados de elevação nas concentrações de proteínas de fase aguda no soro sangüíneo (Fagliari et al, 1998).…”

“…Esse autor propôs a classificação histopatológica das lesões, de acordo com a sua gravidade, em normal (grau N), discreta (grau 1), moderada (grau 2) e grave (grau 3) baseando-se, principalmente, nas alterações da membrana basal. A membrana basal, composta de proteínas colagenosas, como o colágeno tipo IV, e de proteínas não-colagenosas, como proteoglicans e glicoproteínas, das quais a principal é a laminina, é degradada por metaloproteinases (Johnson et al, 2000). Pollitt (1999) considerou a ativação descontrolada de metaloproteinases como importante evento na patogênese da laminite.…”