Structure and Function of Smooth Muscle with Special Reference to Mast Cells

Vodenicharov, A.

doi:10.5772/48566

Cited by 4 publications

(6 citation statements)

References 60 publications

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“…Having in mind the well‐known role of heparin in the inhibition of motility and proliferation of the vascular and myometrial smooth muscle cells (Lake and Castellot, ; Masson et al., ; Fasciano et al., ), it could be presumed a similar role predominates also in the circular smooth layer of the musculus sphincter ductus choledochus . That opinion could also be supported by recently reported data regarding the role of canine and porcine heparin‐positive MCs in the motility of smooth and skeletal muscle cells (Stefanov et al., ; Vodenicharov, ). In this regard, the results of the current study allowed us to suggest the role of MCs in the control of sphincter of Oddi function.…”

Section: Discussionsupporting

confidence: 54%

Histochemical Study of Heparin‐positive Mast Cells in the Terminal Part of Porcine Ductus Choledochus and Papilla Duodeni Major

Stefanov

Vodenicharov

Tsandev

et al. 2015

Anat Histol Embryol

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The study presented in detail the localization and density of mast cells (MCs) in the intramural part of the common bile duct (CBD) and in the major duodenal papilla (MDP) of domestic swine. MCs' density (number/mm(2) ) in different layers of both of the duct and papilla was evaluated after toluidine blue staining. Their number was higher in the lamina propria mucosae than in the tunica muscularis of the studied structures. The localization of berberine-positive, (heparin containing) MCs and the ratio between them and toluidine blue-positive MCs with γ-ma metachromasia was also established. Ratios of heparin-containing MCs in comparison with all toluidine blue-positive MCs were found as follows: ductus choledochus - 32% in the subglandular connective tissue of lamina propria mucosae in the intramural part of the duct; m. sphincter ductus choledochus - 31% in the circular and 0.06% in the longitudinal muscle layer; subserosa - 59%; papilla duodeni major - 0.03% in the subepithelial connective tissue and 34% in the subglandular connective tissue of lamina propria mucosae, respectively. The established large difference in heparin-positive MCs in both the subepithelial and subglandular connective tissues of CBD and MDP, respectively, is an evidence for the existence of mucosal and connective tissue MCs.

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Section: Discussionsupporting

confidence: 54%

Histochemical Study of Heparin‐positive Mast Cells in the Terminal Part of Porcine Ductus Choledochus and Papilla Duodeni Major

Stefanov

Vodenicharov

Tsandev

et al. 2015

Anat Histol Embryol

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“…The structure of smooth muscle tissue is different from that of other muscle tissue subtypes, and the spindle shape of mononucleated smooth muscle cells (SMCs) permits close contact among cells in vessel walls ( Vodenicharov, 2012 ). The thickness of the medial layer, which is composed mainly of SMCs, greatly determines pulmonary artery resistance and pressure ( Siques et al, 2018 ).…”

Section: Pasmcs and Hypobaric Hypoxiamentioning

confidence: 99%

“…Importantly, all layers of the pulmonary artery (the adventitia, smooth muscle, and endothelial cell layers) and the surrounding cells (mast cells, fibroblasts, and macrophages) contribute to or are involved in the development of HAPH ( Vodenicharov, 2012 ; Siques et al, 2018 ). However, some of the principal action sites of HAPH are pulmonary artery smooth muscle cells (PASMCs), which interact with several extracellular and intracellular molecules and participate in diverse mechanisms – based on the evolution and degree of hypoxia – that lead to proliferation, apoptosis, and fibrosis ( Udjus et al, 2019 ).…”

Section: Introductionmentioning

confidence: 99%

Oxidative Stress, Kinase Activation, and Inflammatory Pathways Involved in Effects on Smooth Muscle Cells During Pulmonary Artery Hypertension Under Hypobaric Hypoxia Exposure

2021

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High-altitude exposure results in hypobaric hypoxia, which affects organisms by activating several mechanisms at the physiological, cellular, and molecular levels and triggering the development of several pathologies. One such pathology is high-altitude pulmonary hypertension (HAPH), which is initiated through hypoxic pulmonary vasoconstriction to distribute blood to more adequately ventilated areas of the lungs. Importantly, all layers of the pulmonary artery (adventitia, smooth muscle, and endothelium) contribute to or are involved in the development of HAPH. However, the principal action sites of HAPH are pulmonary artery smooth muscle cells (PASMCs), which interact with several extracellular and intracellular molecules and participate in mechanisms leading to proliferation, apoptosis, and fibrosis. This review summarizes the alterations in molecular pathways related to oxidative stress, inflammation, kinase activation, and other processes that occur in PASMCs during pulmonary hypertension under hypobaric hypoxia and proposes updates to pharmacological treatments to mitigate the pathological changes in PASMCs under such conditions. In general, PASMCs exposed to hypobaric hypoxia undergo oxidative stress mediated by Nox4, inflammation mediated by increases in interleukin-6 levels and inflammatory cell infiltration, and activation of the protein kinase ERK1/2, which lead to the proliferation of PASMCs and contribute to the development of hypobaric hypoxia-induced pulmonary hypertension.

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“…Despite major advances in the role of immune inflammation in the regulation of the structure and function of the smooth muscles in other systems, there is a paucity of work on the gastrointestinal smooth muscles, especially in the esophagus. The relevant findings from other systems suggest the possible signaling pathway for the mechanical stress leading to the pathogenesis of esophageal motility disorders ( 29 , 30 ). Figure 1 lists the steps in the generation of mechanostress and in the progression of mechanostressed smooth muscle-induced functional and structural changes.…”

Section: Effect Of Mechanical Stress On Esophageal Smooth Musclementioning

confidence: 99%

Role of mechanoregulation in mast cell-mediated immune inflammation of the smooth muscle in the pathophysiology of esophageal motility disorders

Goyal,

Rattan

2024

American Journal of Physiology-Gastrointestinal and Liver Physi

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Major esophageal disorders involve obstructive transport of bolus to the stomach, causing symptoms of dysphagia and impaired clearing of the refluxed gastric contents. These may occur due to mechanical constriction of the esophageal lumen or loss of relaxation associated with deglutitive inhibition, as in achalasia-like disorders. Recently, immune inflammation has been identified as an important cause of esophageal strictures and the loss of inhibitory neurotransmission. These disorders are also associated with smooth muscle hypertrophy and hypercontractility, whose cause is unknown. This review investigated immune inflammation in the causation of smooth muscle changes in obstructive esophageal bolus transport. Findings suggest that smooth muscle hypertrophy occurs above the obstruction and is due to mechanical stress on the smooth muscles. The mechanostressed smooth muscles release cytokines and other molecules that may recruit and microlocalize mast cells to smooth muscle bundles, so that their products may have close bidirectional effect on each other. Acting in a paracrine fashion, the inflammatory cytokines induce genetic and epigenetic changes in the smooth muscles, leading to smooth muscle hypercontractility, hypertrophy, and impaired relaxation. These changes may worsen difficulty in the esophageal transport. Immune processes differ in the first phase of obstructive bolus transport, and the second phase of muscle hypertrophy and hypercontractility. Moreover, changes in type of mechanical stress may change immune response and effect smooth muscles. Understanding immune signaling in causes of obstructive bolus transport, type of mechanical stress, and associated smooth muscle changes may help pathophysiology-based prevention and targeted treatment of esophageal motility disorders.

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Structure and Function of Smooth Muscle with Special Reference to Mast Cells

Cited by 4 publications

References 60 publications

Histochemical Study of Heparin‐positive Mast Cells in the Terminal Part of Porcine Ductus Choledochus and Papilla Duodeni Major

Histochemical Study of Heparin‐positive Mast Cells in the Terminal Part of Porcine Ductus Choledochus and Papilla Duodeni Major

Oxidative Stress, Kinase Activation, and Inflammatory Pathways Involved in Effects on Smooth Muscle Cells During Pulmonary Artery Hypertension Under Hypobaric Hypoxia Exposure

Role of mechanoregulation in mast cell-mediated immune inflammation of the smooth muscle in the pathophysiology of esophageal motility disorders

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