scholarly journals The Role of Substance P in Pulmonary Clearance of Bacteria in Comparative Injury Models

2016 ◽  
Vol 186 (12) ◽  
pp. 3236-3245 ◽  
Author(s):  
Terry Hsieh ◽  
Max H. Vaickus ◽  
Thor D. Stein ◽  
Bethany L. Lussier ◽  
Jiyoun Kim ◽  
...  
Keyword(s):  
Substance P ◽  
Pulmonary Clearance ◽  
Injury Models

scholarly journals A9 DORSAL ROOT GANGLIA NEURONAL RESPONSES AND SUBSTANCE P PRODUCTION ARE HIGHER IN MALE MICE

2021 ◽  
Vol 4 (Supplement_1) ◽  
pp. 10-11
Author(s):  
J Pujo ◽  
G De Palma ◽  
J Lu ◽  
S M Collins ◽  
P Bercik
Keyword(s):  
Abdominal Pain ◽  
Substance P ◽  
Gut Microbiota ◽  
Sensory Neurons ◽  
Dorsal Root ◽  
Neuronal Response ◽  
Neuronal Responses ◽  
Visceral Sensitivity ◽  
Germ Free

Abstract Background Abdominal pain is a common complaint in patients with chronic gastrointestinal disorders. Accumulating evidence suggests that gut microbiota is an important determinant of gut function, including visceral sensitivity. Germ-free (GF) mice have been shown to display visceral hypersensitivity, which normalizes after colonization. Sex also appears to play a key role in visceral sensitivity, as women report more abdominal pain than men. Thus, both gut bacteria and sex are important in the regulation of gut nociception, but the underlying mechanisms remain poorly understood. Aims To investigate the role of gut microbiota and sex in abdominal pain. Methods We used primary cultures of sensory neurons from dorsal root ganglia (DRG) of female and male conventionally raised (SPF) or germ-free (GF) mice (7–18 weeks old). To study the visceral afferent activity in vitro, calcium mobilization in DRG sensory neurons was measured by inverted fluorescence microscope using a fluorescent calcium probe Fluo-4 (1mM). Two parameters were considered i) the percentage of responding neurons ii) the intensity of the neuronal response. First, DRG sensory neurons were stimulated by a TRPV1 agonist capsaicin (12.5nM, 125nM and 1.25µM) or by a mixture of G-protein coupled receptors agonist (GPCR: bradykinin, histamine and serotonin; 1µM, 10µM and 100µM). We next measured the neuronal production of substance P and calcitonin gene-related peptide (CGRP), two neuropeptides associated with nociception, in response to capsaicin (1.25µM) or GPCR agonists (100µM) by ELISA and EIA, respectively. Results The percentage of neurons responding to capsaicin and GPCR agonists was similar in male and female SPF and GF mice. However, the intensity of the neuronal response was higher in SPF male compared to SPF female in response to capsaicin (125nM: p=0.0336; 1.25µM: p=0.033) but not to GPCR agonists. Neuronal activation was similar in GF and SPF mice of both sexes after administration of capsaicin or GPCR agonists. Furthermore, substance P and CGRP production by sensory neurons induced by capsaicin or GPCR agonists was similar in SPF and GF mice, regardless of sex. However, while the response to capsaicin was similar, the GPCR agonists-induced production of substance P was higher in SPF male mice compared to SPF females (p=0.003). The GPCR agonists-induced production of CGRP was similar in SPF male and female mice. Conclusions Our data suggest that at the level of DRG neurons, the absence of gut microbiota does not predispose to visceral hypersensitivity. The intensity of DRG neuronal responses to capsaicin and the GPCR agonists-induced production of substance P are higher in male compared to female mice, in contrast to previously published studies in various models of acute and chronic pain. Further studies are thus needed to investigate the role of sex in visceral sensitivity. Funding Agencies CIHR

Role of the C Domain of IGFs in Synergistic Promotion, with a Substance P–Derived Peptide, of Rabbit Corneal Epithelial Wound Healing

2004 ◽  
Vol 45 (4) ◽  
pp. 1125 ◽  
Author(s):  
Naoyuki Yamada ◽  
Ryoji Yanai ◽  
Masatsugu Nakamura ◽  
Makoto Inui ◽  
Teruo Nishida
Keyword(s):  
Wound Healing ◽  
Substance P ◽  
Corneal Epithelial ◽  
Epithelial Wound Healing

Role of substance P in allergic nasal symptoms in rats

2006 ◽  
Vol 532 (1-2) ◽  
pp. 155-161 ◽  
Author(s):  
Md. Ashequr Rahman ◽  
Toshio Inoue ◽  
Chiaki Kamei
Keyword(s):  
Substance P ◽  
Nasal Symptoms

Paradoxical effect of salbutamol in a model of acute organophosphates intoxication in guinea pigs: role of substance P release

2007 ◽  
Vol 292 (4) ◽  
pp. L915-L923 ◽  
Author(s):  
Jaime Chávez ◽  
Patricia Segura ◽  
Mario H. Vargas ◽  
José Luis Arreola ◽  
Edgar Flores-Soto ◽  
...  
Keyword(s):  
Substance P ◽  
Guinea Pigs ◽  
Smooth Muscle Contraction ◽  
In Vivo Experiments ◽  
Intracellular Ca ◽  
Neurokinin 1 ◽  
Substance P Release

Organophosphates induce bronchoobstruction in guinea pigs, and salbutamol only transiently reverses this effect, suggesting that it triggers additional obstructive mechanisms. To further explore this phenomenon, in vivo (barometric plethysmography) and in vitro (organ baths, including ACh and substance P concentration measurement by HPLC and immunoassay, respectively; intracellular Ca2+ measurement in single myocytes) experiments were performed. In in vivo experiments, parathion caused a progressive bronchoobstruction until a plateau was reached. Administration of salbutamol during this plateau decreased bronchoobstruction up to 22% in the first 5 min, but thereafter airway obstruction rose again as to reach the same intensity as before salbutamol. Aminophylline caused a sustained decrement (71%) of the parathion-induced bronchoobstruction. In in vitro studies, paraoxon produced a sustained contraction of tracheal rings, which was fully blocked by atropine but not by TTX, ω-conotoxin (CTX), or epithelium removal. During the paraoxon-induced contraction, salbutamol caused a temporary relaxation of ∼50%, followed by a partial recontraction. This paradoxical recontraction was avoided by the M2- or neurokinin-1 (NK1)-receptor antagonists (methoctramine or AF-DX 116, and L-732138, respectively), accompanied by a long-lasting relaxation. Forskolin caused full relaxation of the paraoxon response. Substance P and, to a lesser extent, ACh released from tracheal rings during 60-min incubation with paraoxon or physostigmine, respectively, were significantly increased when salbutamol was administered in the second half of this period. In myocytes, paraoxon did not produce any change in the intracellular Ca2+ basal levels. Our results suggested that: 1) organophosphates caused smooth muscle contraction by accumulation of ACh released through a TTX- and CTX-resistant mechanism; 2) during such contraction, salbutamol relaxation is functionally antagonized by the stimulation of M2 receptors; and 3) after this transient salbutamol-induced relaxation, a paradoxical contraction ensues due to the subsequent release of substance P.

The role of substance P in the pathogenesis of experimental allergic neuritis

1993 ◽  
Vol 46 (1-2) ◽  
pp. 251-253
Author(s):  
Shujian Wu ◽  
Juan Chen ◽  
Chengtao Xu
Keyword(s):  
Substance P ◽  
Experimental Allergic Neuritis ◽  
Experimental Allergic ◽  
Allergic Neuritis

scholarly journals The role of substance P as a neurotransmitter in the reflexes of slow time courses in the neonatal rat spinal cord

1985 ◽  
Vol 84 (3) ◽  
pp. 663-673 ◽  
Author(s):  
Hiroyuki Akagi ◽  
Shiro Konishi ◽  
Masanori Otsuka ◽  
Mitsuhiko Yanagisawa
Keyword(s):  
Spinal Cord ◽  
Substance P ◽  
Neonatal Rat ◽  
Rat Spinal Cord ◽  
Slow Time ◽  
Time Courses

Synthesis of a Substance P Antagonist with a Somatostatin Scaffold:  Factors Affecting Agonism/Antagonism at GPCRs and the Role of Pseudosymmetry

2000 ◽  
Vol 43 (21) ◽  
pp. 3827-3831 ◽  
Author(s):  
Josephine Liu ◽  
Dennis J. Underwood ◽  
Margaret A. Cascieri ◽  
Susan P. Rohrer ◽  
Louis-David Cantin ◽  
...  
Keyword(s):  
Substance P ◽  
Factors Affecting ◽  
Substance P Antagonist

The role of lateral septal NK1 receptors in mediating anxiogenic effects induced by intracerebroventricular injection of substance P

2002 ◽  
Vol 134 (1-2) ◽  
pp. 411-415 ◽  
Author(s):  
E.C Gavioli ◽  
N.S Canteras ◽  
T.C.M De Lima
Keyword(s):  
Substance P ◽  
Intracerebroventricular Injection ◽  
Nk1 Receptors

Abstract 060: CCN1/a 6 β 1 Mediates Myocardial Injuries Induced by Work Overload or by Doxorubicin in Mice

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Pei-Ling I Hsu ◽  
Fan-E Mo
Keyword(s):  
Myocardial Injury ◽  
Fas Ligand ◽  
Cardiac Injury ◽  
Pressure Overload ◽  
Myocardial Damage ◽  
Matricellular Protein ◽  
Work Overload ◽  
Myocardial Injuries ◽  
Injury Models

Introduction: Matricellular protein CCN1 is expressed in myocardial infarction, pressure overload, and ischemia in mice, and in patients with a failing heart. Despite its well-documented angiogenic activities, CCN1 promotes fibroblast apoptosis in some contexts. The role of CCN1 in an injured heart was not clear. We assessed the hypothesis that CCN1 plays a detrimental role and mediates cardiac injury through its proapoptotic activities. Methods and Results: To test the role of CCN1 in cardiac injury, we employed two different myocardial injury models in mice, including a work-overload-induced injury created by isoproterenol treatment (ISO; 100 mg/kg/day; s.c. for 5 days; n= 6 for each group) and an injury induced by the cardiotoxicity of doxorubicin (DOX, single dose of 15 mg/kg; i.p. sacrificed after 14 days). Ccn1 expression was induced in the damaged myocardium in both injury models. A line of knock-in mice carrying an apoptosis-defective Ccn1 mutant allele, Ccn1-dm , which has disrupted integrin α 6 β 1 binding sites, were tested in the ISO- or DOX -induced cardiac injury. Myocardial damage was seen in tissues from wile-type (WT) hearts after receiving ISO. Ccn1 dm/dm (DM) mice possessed remarkable resistance against ISO or DOX treatments and exhibited no tissue damage or fibrosis compared to WT mice after H&E or Masson’s trichrome stainings. DM mice were resistant to both ISO- and DOX-induced cardiac cell apoptosis, indicating that CCN1 is critically mediating cardiomyocyte apoptotic death in cardiac injury. Moreover, we found that death factor Fas ligand (FasL) and its receptor Fas were upregulated in WT mice receiving ISO or DOX treatments by immunohistochemical staining, compared with the PBS-control. 8-OHdG-positive, a marker for oxidative stress, cardiomyocytes were increased by ISO or DOX treatments as well. In contrast, the expression of Fas/FasL, and the 8-OHdG-positive cardiomyocytes in the myocardium of DM mice were not changed by ISO or DOX. Conclusions: We identify CCN1 as a novel pathophysiological regulator of cardiomyocyte apoptosis in cardiac injury. Blocking apoptotic function of CCN1 effectively prevents myocardial injury in mice. CCN1 and its receptor α 6 β 1 represent promising future therapeutic targets in cardiac injury.

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