Isobaric tags for relative and absolute quantification-based proteomic analysis that reveals the roles of progesterone receptor, inflammation, and fibrosis for slow-transit constipation

2018 ◽  
Vol 33 (2) ◽  
pp. 385-392 ◽  
Author(s):  
Yuwei Li ◽  
Yongjun Yu ◽  
Shuyuan Li ◽  
Mingqing Zhang ◽  
Zhao Zhang ◽  
...  
Keyword(s):  
Progesterone Receptor ◽  
Proteomic Analysis ◽  
Absolute Quantification ◽  
Slow Transit Constipation ◽  
Slow Transit ◽  
Isobaric Tags ◽  
Transit Constipation

Proteomic analysis of down-regulated proteins in colonic mucosa of chronic slow transit constipation rats

2009 ◽  
Vol 24 (3) ◽  
pp. 136-141 ◽  
Author(s):  
Wang Xingwei ◽  
Liu Haifeng ◽  
Xu Mei ◽  
Chen Gang ◽  
He Juntang ◽  
...  
Keyword(s):  
Proteomic Analysis ◽  
Colonic Mucosa ◽  
Slow Transit Constipation ◽  
Slow Transit ◽  
Transit Constipation

Progesterone receptor A mediates VIP inhibition of contraction

2010 ◽  
Vol 298 (3) ◽  
pp. G433-G439 ◽  
Author(s):  
Ling Cheng ◽  
Piero Biancani ◽  
Jose Behar
Keyword(s):  
Progesterone Receptor ◽  
Guinea Pig ◽  
Western Blot ◽  
G Proteins ◽  
Muscle Cells ◽  
Slow Transit Constipation ◽  
Protein Levels ◽  
Human Control ◽  
Slow Transit ◽  
Transit Constipation

The slow transit time of the colon in females with constipation is due to impairment of agonist-induced contraction. The impairment is associated with downregulation of G proteins that mediate contraction and upregulation of Gs proteins that mediate relaxation. These changes are caused by overexpression of progesterone (P4) receptors in the colon, rendering its muscle cells sensitive to physiological P4 concentrations. Downregulation of Gq/11 is mediated by P4 receptor B (PR-B). We examined whether upregulation of Gs proteins increased the inhibition of contraction and whether the increase is mediated by the P4 receptor A (PR-A). These studies were conducted in colon-isolated colon muscle cells from human control and slow-transit constipation (STC) females and from guinea pigs. Muscle cell contraction was induced by CCK-8. Inhibition of contraction was induced by vasoactive intestinal polypeptide (VIP), and 8′bromo-c′AMP (8B-c′AMP) G protein levels were determined by Western blot. VIP-induced inhibition of contraction was greater in muscle cells from STC and P4-treated muscle cells. There were no differences in the inhibition induced by 8B-c′AMP between muscle cells from STC and P4-treated controls. The increased VIP-induced inhibition of muscle cells treated with P4 was blocked by pretreatment with PR-A antibodies and unaffected by PR-B antibodies. These antibodies had no effect on 8B-c′AMP induced-inhibition. The P4 upregulation of Gs proteins was blocked by PR-A antibodies and unaffected by PR-B antibodies. Similar results were obtained in muscle cells from guinea pig colons. We concluded that P4 upregulation of Gs proteins increases VIP-induced inhibition of contraction mediated by PR-A.

Autoimmune encephalitis and gastrointestinal dysmotility: achalasia, gastroparesis, and slow transit constipation

2020 ◽  
Vol 58 (10) ◽  
pp. 975-981
Author(s):  
Thomas Frieling ◽  
Christian Kreysel ◽  
Michael Blank ◽  
Dorothee Müller ◽  
Ilka Melchior ◽  
...  
Keyword(s):  
Interstitial Cells Of Cajal ◽  
Autoimmune Encephalitis ◽  
Enteric Neurons ◽  
Slow Transit Constipation ◽  
Gastrointestinal Dysmotility ◽  
Slow Transit ◽  
Small Intestinal ◽  
Interdigestive Motility ◽  
Cells Of Cajal ◽  
Transit Constipation

Abstract Background Neurological autoimmune disorders (NAD) are caused by autoimmune inflammation triggered by specific antibody subtypes. NAD may disturb the gut-brain axis at several levels including brain, spinal cord, peripheral, or enteric nervous system. Case report We present a case with antinuclear neuronal Hu (ANNA-1)- and antiglial nuclear (SOX-1) autoimmune antibody-positive limbic encephalitis and significant gastrointestinal dysmotility consisting of achalasia type II, gastroparesis, altered small intestinal interdigestive motility, and severe slow transit constipation. The autoantibodies of the patient’s serum labeled enteric neurons and interstitial cells of Cajal but no other cells in the gut wall. Achalasia was treated successfully by pneumatic cardia dilation and gastrointestinal dysmotility successfully with prucalopride. Conclusion NAD may disturb gastrointestinal motility by altering various levels of the gut-brain axis.

scholarly journals Prevalence and Clinical Characteristics of Dyssynergic Defecation and Slow Transit Constipation in Patients with Chronic Constipation

2021 ◽  
Vol 10 (9) ◽  
pp. 2027
Author(s):  
Samuel Tanner ◽  
Ahson Chaudhry ◽  
Navneet Goraya ◽  
Rohan Badlani ◽  
Asad Jehangir ◽  
...  
Keyword(s):  
Medical History ◽  
Chronic Constipation ◽  
Clinical Characteristics ◽  
Anorectal Function ◽  
Slow Transit Constipation ◽  
Dyssynergic Defecation ◽  
Patient Demographics ◽  
Balloon Expulsion ◽  
Slow Transit ◽  
Transit Constipation

Patients with chronic constipation who do not respond to initial treatments often need further evaluation for dyssynergic defecation (DD) and slow transit constipation (STC). The aims of this study are to characterize the prevalence of DD and STC in patients referred to a motility center with chronic constipation and correlate diagnoses of DD and STC to patient demographics, medical history, and symptoms. High-resolution ARM (HR-ARM), balloon expulsion testing (BET) and whole gut transit scintigraphy (WGTS) of consecutive patients with chronic constipation were reviewed. Patients completed questionnaires describing their medical history and symptoms at the time of testing. A total of 230 patients completed HR-ARM, BET, and WGTS. Fifty (22%) patients had DD, and 127 (55%) patients had STC. Thirty patients (13%) had both DD and STC. There were no symptoms that were suggestive of STC vs. DD; however, patients with STC and DD reported more severe constipation than patients with normal transit and anorectal function. Patients with chronic constipation often need evaluation for both DD and STC to better understand their pathophysiology of symptoms and help direct treatment.

Sacral nerve stimulation for idiopthic slow transit constipation

2000 ◽  
Vol 118 (4) ◽  
pp. A848 ◽  
Author(s):  
Andrew J. Malouf ◽  
Paul H. Wiesel ◽  
Tanya Nicholls ◽  
R. John Nicholls ◽  
Michael A. Kamm
Keyword(s):  
Nerve Stimulation ◽  
Sacral Nerve Stimulation ◽  
Slow Transit Constipation ◽  
Sacral Nerve ◽  
Slow Transit ◽  
Transit Constipation
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