Innervation of the sinusoidal wall: Regulation of the sinusoidal diameter

Abstract

In the livers of humans, cats, guinea pigs, and tupaia, nerve endings are distributed all over the hepatic lobules. Nerve endings in the intralobular spaces are localized mainly in the Disse spaces and are oriented toward the hepatic stellate cells (HSCs), sinusoidal endothelial cells, and hepatocytes. They are especially closely related to HSCs. Various neurotransmitters such as substance P exist in the nerve endings. In addition, HSCs possess endothelin (ET) and adrenergic receptors and contract in response to the corresponding agonists. In contrast, nitric oxide (NO) inhibits the contraction of HSCs. HSCs thus appear to be involved in the regulation of hepatic sinusoidal microcirculation by contraction and relaxation. In the cirrhotic liver, intralobular innervation is decreased, but ET, ET receptors, and NO are overexpressed in the HSCs. These findings indicate that HSCs in cirrhotic liver may play an important role in the sinusoidal microcirculation through agents such as ET or NO rather than through intralobular innervation.

Perineuroma of the skin negative for S100 protein but positive for stem cell antigens: A possible stem cell tumor

“…[11][12][13][14][15][16][17][18][19][20][21][22][23][24][25][26][27] These findings strongly suggest the close association between the present tumor and neural stem cells. [11][12][13][14][15][16][17][18][19][20][21][22][23][24][25][26][27] It can be plausible that the present tumor arose from neural stem cells. That is, there is a possibility that the present tumor is a kind of stem cell tumor.…”

“…These findings suggest that stem cell factor/KIT, platelet-derived growth factor-alpha/PDGFRA, hepatocyte growth factor/MET, and epidermal growth factor/ErbB2 signaling pathways play an important role in the tumorigenesis and tumor growth in the present perineuroma. [11][12][13][14][15][16][17][18][19][20][21][22][23][24][25][26][27] In the present case, CK14 (a stem cell antigen) was negative, suggesting that all stem cell markers are not expressed in the present possible stem cell tumors. The present tumor showed negative expression of CK AE1/3, CK CAM5.2 and EMA, indicating that the present tumor is not an epithelial tumor.…”

Sinusoidal Obstruction Syndrome (Hepatic Veno-Occlusive Disease)

“…34 In the second instance, nitric oxide levels in the hepatic vein of rats decrease during induction of SOS, 35 and induction of SOS can either be exacerbated by administration of N(G)-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide synthase, or be mitigated by infusion of V-YRRO/NO, a liver-selective nitric oxide donor prodrug, 36 Beyond providing evidence for nitric oxide depletion in the pathogenesis of SOS, 35 a role for vasoconstriction also is implicated, since adequate nitric oxide levels inhibit vasoconstriction of hepatic stellate cells, which invest the hepatic sinusoidal from within the space of Disse. 37 Matrix metalloproteinase-9 expression increases early in the rat monocrotaline-induced SOS model; later there is a lower magnitude increase in matrix metalloproteinase-2. SECs are the major source of both basal and monocrotaline-induced enzyme expression and release.…”

Mechanisms of adaptation of the hepatic vasculature to the deteriorating conditions of blood circulation in liver cirrhosis

“…Substances for instance endothelin1, substance P, angiotensin Ⅱ, norepinephrine, prosta glandin F2, thromboxane A2, platelet activating factor (PAF) and thrombin can trigger HSC contractility. In contrast, vasoactive substances such as acetylcholine, vasoactive intestinal peptide, NO, carbon monoxide, hydrogen sulfide, prostaglandin E2, and adrenomedullin are known for the ability to relax HSCs [5] . independent pathway, Rho kinase and protein kinase C inhibit the activity of myosin light chain phosphatase, an enzyme that depho sphorylates phosphorylated myosin light chains and induces relaxation [6] .…”