Smooth Myocytes - Tissue Functioning and Remodeling in the Circulatory and Ventilatory Systems - page 419

Table 8.13. Membrane carriers with regulation factors for mechanosensitive carriers (PKA:
cAMP-dependent protein kinase; PKG: cGMP-dependent protein kinase; Sources: [ 762 , 771 ]).

Type Regulation

Active transporters
Na + -K + ATPase Na + ] K + ] PKC, PKA, [ i , [ e

Ca 2 + AT P a s e C a m , P K G

K + -H + AT P a s e

Cotransporters
Na + -Cl − -HCO 3
Na + -K + -Cl −
Cl − -HCO 3

Exchangers

Na + -H +
Na + -Ca 2 + PKC, PKG

myocytes constitutively synthesize and secrete MMP2, but MMP9 production is
inducible under the control of NF B factor. These cells also fabricate MMP3 42

and MMP7 peptidases. 43 Vascular smooth myocytes secrete MMPs as inactive
precursors. Plasmin activates proMMPs.
Vascular smooth myocytes produce tissue peptidase inhibitors . They also consti-
tutively express and secrete several serine peptidases such as tissue-type plasmino-
gen activator (tPA); tPA synthesis can be enhanced by numerous stimuli.
Like any cell type, vascular smooth myocytes manufacture intracellular cysteine
peptidases associated with phagolysosomes. On the plasma membrane, cathepsin-
G colocalizes with

κ

α V β 3 -integrin. It participates in vSMC migration. Unlike other
cathepsin types, cathepsin-S can be secreted and act in the extracellular milieu
at neutral pH. Inducible cathepsin-S synthesis is triggered by IL1 β and other

cytokines.

8.5.5.3 Clearance of Blood-Conveyed Proteases

Blood plasminogen is a zymogen secreted by the liver. It circulates at a mi-
cromolar concentration and can be convected through the vascular wall. Tissue
plasminogen activator that, together with plasminogen, binds to Lys residues of the
annexin-A2-S100a10 heterotetramer on the vSMC surface and forms an activator
for plasmin [ 745 ]. Pericellular plasmin degrades fibronectin and causes vSMC

42 A.k.a. stromelysin-1.
43 A.k.a. matrilysin-1.