Relationship between overexpression of NK-1R, NK-2R and intestinal mucosal damage in acute necrotizing pancreatitis

Shi, Xin; Nai-rong, Gao; Guo, Qingming; Yang, Yongpeng; Huo, Mingdong; Hu, Hailong; Friess, Helmut

doi:10.3748/wjg.v9.i1.160

Cited by 13 publications

(10 citation statements)

References 40 publications

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“…Collectively, these studies suggest that SP has a primary role in tissue repair. Although Bowden et al (38) report NK-l receptors to be internalized on SP binding, (39) there are published studies suggesting NK-l receptors to be upregulated on activation (39)(40)(41). Data presented here that indicate increased NK-I receptor immunoreactivity after the exogenous addition of SP are consistent with the conclusions of Velazquez et al (40), who suggest an SP-mediated upregulation in rat spinal cord.…”

Section: So -'-"supporting

confidence: 88%

Exogenous Administration of Substance P Enhances Wound Healing in a Novel Skin-Injury Model

Delgado

McManus

Chambers

2005

Exp Biol Med (Maywood)

102

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Soft tissue injury accounts for approximately 44% of all wounds in both the military and civilian populations. Following injury to soft tissue, Substance P (SP) and other neuropeptides are released by cutaneous neurons and modulate the function of immunocompetent and inflammatory cells, as well as epithelial and endothelial cells. The interaction between these components of the nervous system and multiple target cells affecting cutaneous repair is of increasing interest. In this report, we describe the effects of SP on wound repair in a novel, laser-induced, skin-wound model. Gross and histologic examination of laser-induced injury revealed that exogenously administered SP affects wound healing via neurite outgrowth, in addition to adhesion molecule and neurokinin-1 receptor involvement in vivo. All SP effects were decreased by pretreatment with Spantide II, an SP antagonist. The elucidation of SP-mediating mechanisms is crucial to firmly establishing the involvement and interaction of the peripheral nervous system and the immune system in cutaneous repair. Findings presented here suggest that SP participates in the complex network of mediators involved in cutaneous inflammation and wound healing.

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Section: So -'-"supporting

confidence: 88%

Exogenous Administration of Substance P Enhances Wound Healing in a Novel Skin-Injury Model

Delgado

McManus

Chambers

2005

Exp Biol Med (Maywood)

102

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“…The real‐time RT‐PCR for NK‐1R mRNA was carried out with the Brilliant SYBR Green QPCP Master Mix (Bio‐Rad Laboratories, Hercules, CA). The specific oligonucleotide primers used were as follows: Rat NK‐1R: 5′‐CAT CAA CCC AGA TCT CTA CC‐3′ (sense) and 5′‐GCT GGA GCT TTC TGT CAT GGA‐3′ (anti‐sense) (Shi X, 2003); Rat MOR: 5′‐ GGT ACT GGG AGA ACC TGC TCA AAA TCT GTG‐3′ (sense) and 5′‐ GTT CCC TAG TGT TCT GAC GGA CTC GAG TGG ‐3′ (anti‐sense); Rat HPRT (a rat house keeping gene) : 5′‐ TCC TGT TGA TGT GGC CAG TAA A‐3′ (sense) and 5′ ‐ GGA CGG AGC AAC AGA CAT TTC T‐3′ (anti‐sense). The oligonucleotide primers were synthesized by Integrated DNA Technologies Inc. (Coralville, IA).…”

Section: Methodsmentioning

confidence: 99%

Morphine upregulates functional expression of neurokinin‐1 receptor in neurons

Wan

Douglas

Wang

et al. 2006

J of Neuroscience Research

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Neuronkinin-1 receptor (NK-1R), the neuropeptide substance P (SP) preferring receptor, is highly expressed in areas of the central nervous system (CNS) that are especially implicated in depression, anxiety, and stress. Repeated exposure to opioids may sensitize neuronal systems involved in stress response. We examined the effects of morphine, the principal metabolite of heroin, on the functional expression of NK-1R in the cortical neurons. NK-1R and mu-opioid receptor (MOR) are co-expressed in the cortical neurons. Morphine enhanced NK-1R expression in the cortical neurons at both the mRNA and protein levels. The upregulated NK-1R by morphine had functional activity, because morphine-treated cortical neurons had greater SP-induced Ca(2+) mobilization than untreated neurons. Blocking opioid receptors on the cortical neurons by naltrexone or CTAP (a mu-opioid receptor antagonist) abolished the morphine action. Investigation of the mechanism(s) responsible for the morphine action showed that morphine activated NK-1R promoter and induced the phosphorylation of p38 MAPK protein in the cortical neurons. These in vitro data provide a plausible cellular mechanism for opioid-mediated neurological disorders.

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“…This is associated with multiple systemic complications, such as pulmonary, renal, and cardiovascular failure [9][10][11][12][13][14][15][16][17][18] . Despite considerable improvements in understanding of the pathophysiologic mechanisms and management of these patients, mortality of SAP remains between 15-50 % [19][20][21][22] . Organ failure is a severe complication of SAP and death occurs usually only in patients with SAP and is commonly associated with failure of at least one organ system [23][24][25] .…”

Section: Introductionmentioning

confidence: 99%