IL-1β inhibits intestinal smooth muscle proliferation in an organ culture system: involvement of COX-2 and iNOS induction in muscularis resident macrophages

2007 ◽  
Vol 292 (5) ◽  
pp. G1315-G1322 ◽  
Author(s):  
Takashi Ohama ◽  
Masatoshi Hori ◽  
Eiichi Momotani ◽  
Margaret Elorza ◽  
William T. Gerthoffer ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Organ Culture ◽  
Smooth Muscle Cells ◽  
Muscle Tissue ◽  
Culture System ◽  
Intestinal Inflammation ◽  
Muscle Cells ◽  
No Synthase ◽  
Smooth Muscle Tissue ◽  
Organ Culture System

Intestinal inflammation causes hyperplasia of smooth muscle that leads to thickening of the smooth muscle layer, resulting in dysmotility. IL-1β is a proinflammatory cytokine that plays a central role in intestinal inflammation. In this study, to evaluate the effect of IL-1β on proliferation of ileal smooth muscle cells in vivo, we utilized an organ culture system. When rat ileal smooth muscle tissue was cultured under serum-free conditions for 3 days, most smooth muscle cells maintained their arrangement and kept their contractile phenotype. When 10% FBS was added, an increased number of smooth muscle cells per unit area was observed. Moreover, immunohistochemical staining for PCNA demonstrated that FBS induced proliferation of smooth muscle cells. IL-1β inhibited the proliferative effect of FBS. Furthermore, IL-1β upregulated inducible nitric oxide (NO) synthase and cyclooxygenase-2 mRNA and protein and thus stimulated NO and PGE2productions. Moreover, exogenously applied NO and PGE2inhibited the increase of bromodeoxyuridine-positive cells stimulated with FBS. Immunostaining revealed that the majority of cyclooxygenase-2 and inducible NO synthase was located in the dense network of macrophages resident in the muscularis, which were immunoreactive to ED2. Based on these findings, IL-1β acts as an anti-proliferative mediator, which acts indirectly through the production of PGE2and NO from resident macrophage within ileal smooth muscle tissue.

scholarly journals ARCHITECTURE AND NERVE SUPPLY OF MAMMALIAN SMOOTH MUSCLE TISSUE

1957 ◽  
Vol 3 (6) ◽  
pp. 867-878 ◽  
Author(s):  
Rudolf Caesar ◽  
George A. Edwards ◽  
Helmut Ruska
Keyword(s):  
Endoplasmic Reticulum ◽  
Smooth Muscle ◽  
Plasma Membrane ◽  
Smooth Muscle Cells ◽  
Muscle Cell ◽  
Muscle Tissue ◽  
Plasma Membranes ◽  
Muscle Cells ◽  
Autonomic Nerves ◽  
Smooth Muscle Tissue

Smooth muscle tissue from mouse urinary bladder, uterus, and gall bladder has been studied by means of the electron microscope. The smooth muscle cells are distinctly and completely separated from each other by a cytolemma comparable to the sarcolemma of striated muscle. The tissue is thus cellular and not syncytial. With this evidence, supported by electron microscopy of other tissues, we question the existence of true syncytia in animal tissues. Individual cell membranes necessary for the electrophysiologic events exist in smooth muscle, and its nerve and conduction in a tissue such as uterus or bladder can occur at the cellular level as well as at the tissue area level. The smooth muscle cell contains myofilaments, nucleus, endoplasmic reticulum, mitochondria, Golgi complex, centrosome, and pinocytotic vesicles. These structures are described in some detail, and their probable interrelations and functions are discussed. The autonomic nerves innervating smooth muscle cells are composed of axons and lemnoblasts. The axon is suspended by the mesaxon formed by the infolded plasma membrane of the lemnoblast. The respective plasma membranes separate axon and lemnoblast from each other and from surrounding muscle cells. The axons of autonomic nerves never penetrate the plasma membrane of the muscle cell, but pass or intrude into muscle cell pockets, forming a contact between axonal plasma membrane and smooth muscle plasma membrane. The lemnoblast shows well developed endoplasmic reticulum with Palade granules, mitochondria, and a long, elliptical nucleus. The axon contains neurofilaments, mitochondria, and synaptic vesicles; the quantity of the latter two being significantly greater in the periphery of lemnoblasts and near axon-muscle contact regions. We regard the contact regions as the synapses between the autonomic nerves and the smooth muscle cells.

Axial Stretch Increases Cell Proliferation in Arteries in Organ Culture

2000 ◽  
Author(s):  
Hai-Chao Han ◽  
Raymond P. Vito ◽  
Kristin Michael ◽  
David N. Ku
Keyword(s):  
Cell Proliferation ◽  
Smooth Muscle ◽  
Organ Culture ◽  
Vascular Function ◽  
Culture System ◽  
Carotid Arteries ◽  
Ex Vivo ◽  
Axial Stretch ◽  
Organ Culture System ◽  
Physiological Flow

Abstract To study the effect of axial stretch on vascular function and wall remodeling, porcine carotid arteries were cultured under conditions of physiological flow and elevated axial stretch in an ex vivo organ culture system. Smooth muscle cell proliferation was measured by bromodeoxyuridine index. Results showed that cell proliferation was significantly increased in the highly stretched arteries when compared to the normally stretched arteries. This may indicate the feasibility of stimulating new arterial growth by stretching natural arteries.

cAMP response of vascular smooth muscle cells to bovine parathyroid hormone

1984 ◽  
Vol 247 (6) ◽  
pp. E822-E826 ◽  
Author(s):  
R. C. Stanton ◽  
S. B. Plant ◽  
D. A. McCarron
Keyword(s):  
Smooth Muscle ◽  
Parathyroid Hormone ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Base Line ◽  
Cellular Mechanisms ◽  
Smooth Muscle Tissue ◽  
Camp Content

Parathyroid hormone (PTH) is a vasodilator of vascular smooth muscle tissue. It has been shown to produce this vasodilation in normotensive and hypertensive laboratory rats. The effect is log dose dependent, maximal at 1 min and persists for 3–5 min. The cellular mechanisms involved in PTH-mediated vasodilation are unknown. In this study, we sought to determine the cellular changes of cAMP after administration of bovine (b)PTH (1–34). cAMP content of vascular smooth muscle cells was measured at 30 s, 1, 3, and 5 min after incubation with synthetic bPTH (1–34). Tissue cAMP content was decreased by 55% at 1 min (4.1 +/- 0.5 pmol/mg protein at time 0 vs. 1.9 +/- 0.2 pmol/mg protein at 1 min, P less than 0.001). After 5 min, cAMP levels returned to base-line values and increased over the next 5–10 min to levels above base line (P less than 0.01). In conclusion, our data suggest that the initial response of vascular smooth muscle cells to short-term incubation with bPTH (1–34) is an acute decrease in cAMP content.

scholarly journals Intestinal inflammation downregulates smooth muscle CPI-17 through induction of TNF-α and causes motility disorders

2007 ◽  
Vol 292 (5) ◽  
pp. G1429-G1438 ◽  
Author(s):  
Takashi Ohama ◽  
Masatoshi Hori ◽  
Eiichi Momotani ◽  
Yoichiro Iwakura ◽  
Fengling Guo ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Muscle Tissue ◽  
Proinflammatory Cytokines ◽  
Knockout Mice ◽  
Intestinal Inflammation ◽  
In Vivo Model ◽  
Dependent Manner ◽  
Smooth Muscle Tissue ◽  
Motility Disorders ◽  
Tnf Α

Motility disorders are frequently observed in intestinal inflammation. We previously reported that in vitro treatment of intestinal smooth muscle tissue with IL-1β decreases the expression of CPI-17, an endogenous inhibitory protein of smooth muscle serine/threonine protein phosphatase, thereby inhibiting contraction. The present study was performed to examine the pathophysiological importance of CPI-17 expression in the motility disorders by using an in vivo model of intestinal inflammation and to define the regulatory mechanism of CPI-17 expression by proinflammatory cytokines. After the induction of acute ileitis with 2,4,6,-trinitrobenzensulfonic acid, CPI-17 expression declined in a time-dependent manner. This decrease in CPI-17 expression was parallel with the reduction of cholinergic agonist-induced contraction of smooth muscle strips and sensitivity of permeabilized smooth muscle fibers to Ca2+. Among the various proinflammatory cytokines tested, TNF-α and IL-1β were observed to directly inhibit CPI-17 expression and contraction in cultured rat intestinal tissue. Moreover, both TNF-α and IL-1β inhibited CPI-17 expression and contraction of smooth muscle tissue isolated from wild-type and IL-1α/β double-knockout mice. However, IL-1β treatment failed to inhibit CPI-17 expression and contraction in TNF-α knockout mice. In β-escin-permeabilized ileal tissues, pretreatment with anti-phosphorylated CPI-17 antibody inhibited the carbachol-induced Ca2+ sensitization in the presence of GTP. These findings suggest that CPI-17 was downregulated during intestinal inflammation and that TNF-α plays a central role in this process. Downregulation of CPI-17 may play a role in motility impairments in inflammation.

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