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Novel smooth muscle markers reveal abnormalities of the intestinal musculature in severe colorectal motility disorders
Author(s) -
Wedel T.,
Van Eys G. J. J. M.,
Waltregny D.,
Glénisson W.,
Castronovo V.,
Vanderwinden Jm.
Publication year - 2006
Publication title -
neurogastroenterology and motility
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.489
H-Index - 105
eISSN - 1365-2982
pISSN - 1350-1925
DOI - 10.1111/j.1365-2982.2006.00781.x
Subject(s) - interstitial cell of cajal , pathology , motility , myofilament , myosin , biology , myocyte , myosin light chain kinase , medicine , anatomy , immunohistochemistry , endocrinology , microbiology and biotechnology
Histopathological studies of gastrointestinal motility disorders have mainly focused on enteric nerves and interstitial cells of Cajal, but rarely considered the enteric musculature. Here we used both classical and novel smooth muscle markers and transmission electron microscopy (TEM) to investigate muscular alterations in severe colorectal motility disorders. Full‐thickness specimens from Hirschsprung's disease, idiopathic megacolon, slow‐transit constipation and controls were stained with haematoxylin/eosin (HE) and Masson's trichrome (MT), incubated with antibodies against smooth muscle α ‐actin ( α ‐SMA), smooth muscle myosin heavy chain (SMMHC), smoothelin (SM) and histone deacetylase 8 (HDAC8) and processed for TEM. Control specimens exhibited homogeneous immunoreactivity for all antibodies. Diseased specimens showed normal smooth muscle morphology by HE and MT. While anti‐ α ‐SMA staining was generally normal, immunoreactivity for SMMHC, HDAC8 and/or SM was either absent or focally lacking in Hirschsprung's disease (80%), idiopathic megacolon (75%) and slow‐transit constipation (70%). Ultrastructurally, clusters of myocytes with noticeably decreased myofilaments were observed in all diseases. SMMHC and the novel smooth muscle markers SM and HDAC8 often display striking abnormalities linked to the smooth muscle contractile apparatus unnoticed by both routine stainings and α ‐SMA, suggesting specific defects of smooth muscle cells involved in the pathogenesis of gastrointestinal motility disorders.