Differential expression of Cathepsin S and X in the spinal cord of a rat neuropathic pain model

Abstract

Background: Ample evidence suggests a substantial contribution of cellular and molecular changes in the spinal cord to the induction and persistence of chronic neuropathic pain conditions. While for a long time, proteases were mainly considered as protein degrading enzymes, they are now receiving growing interest as signalling molecules in the pain pathology. In the present study we focused on two cathepsins, CATS and CATX, and studied their spatiotemporal expression and activity during the development and progression of neuropathic pain in the CNS of the rat 5 th lumbar spinal nerve transection model (L5T).

Upregulation of cathepsin S in psoriatic keratinocytes

“…Expression analyses of these enzymes revealed that some matrix metalloproteases and serine proteases (44)(45)(46)(47) add to the list of upregulated proteases in psoriatic keratinocytes. Thus, we can summarize that similar to other tissues (11)(12)(13)48,49), inflammatory changes in the skin are accompanied by a strong induction of CATS.…”

“…Nevertheless, CATS also appears to be expressed in a number of non-immune cells, like neurons, endothelial cells and vascular smoothmuscle cells (11)(12)(13)(14)(15). With respect to the skin CATS was only detected in cell cultures, the human keratinocyte cell line HaCaT and freshly isolated human keratinocytes (16).…”

Increased Immunoreactivity of Cathepsins in the Rat Esophagus under Chronic Acid Reflux Esophagitis

“…In various types of brain injuries, several lysosomal cysteine proteinases, such as CC, CX and CS, are upregulated in microglia/macrophages (Leichsenring et al 2008;Wendt et al 2008;Koike et al 2013b). Moreover, more macrophages had infiltrated in the ulcerated regions than in the non-erosive regions.…”

there any association of metabolic disturbances with joint destruction and pain?

“…Боль, сопровождающаяся воспалением в коленном суставе, может быть связана с разрушением хряща и обусловлена продукцией хондроцитами цитокинов, таких, как TNFα, IL-1β, IL-6 и NGF, которые усиливают деструкцию хряща и индуцируют гипералгезию. В частности, показано, что повышение экспрессии цитокинов IL-1β [169] и COX 1/2 [170] приводило к деградации хряща, экспрессии протеиназ ММР-9, MMP-2, катепсинов К и S [171,172] и усилению боли. Кроме того, TNFα способен непосредственно активировать сенсорные нейроны через свои рецепторы и инициировать каскад провоспалительных реакций, продуцируя интерлейкины [173].…”