Substance P induces expression of the corticotropin-releasing factor receptor 1 by activation of the neurokinin-1 receptor

Hamke, Maike; Herpfer, Inga; Lieb, Klaus; Wandelt, Carolin; Fiebich, Bernd L.

doi:10.1016/j.brainres.2006.03.026

Cited by 26 publications

(20 citation statements)

References 54 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…CRH can activate microglia through CRH R and release inflammatory mediators (Kritas et al, 2014b). Moreover, SP is known to induce the expression of CRH in glia (Hamke et al, 2006). Emotional/chronic stress enhance glial activation and exacerbates neuronal death through inflammation in the substantia nigra of the PD brain (De Pablos et al, 2014).…”

Section: Neuropeptides Sp and Crh In Neuroinflammationmentioning

confidence: 99%

Brain and Peripheral Atypical Inflammatory Mediators Potentiate Neuroinflammation and Neurodegeneration

Kempuraj

Thangavel

Selvakumar

et al. 2017

Front. Cell. Neurosci.

359

265

View full text Add to dashboard Cite

Neuroinflammatory response is primarily a protective mechanism in the brain. However, excessive and chronic inflammatory responses can lead to deleterious effects involving immune cells, brain cells and signaling molecules. Neuroinflammation induces and accelerates pathogenesis of Parkinson’s disease (PD), Alzheimer’s disease (AD) and Multiple sclerosis (MS). Neuroinflammatory pathways are indicated as novel therapeutic targets for these diseases. Mast cells are immune cells of hematopoietic origin that regulate inflammation and upon activation release many proinflammatory mediators in systemic and central nervous system (CNS) inflammatory conditions. In addition, inflammatory mediators released from activated glial cells induce neurodegeneration in the brain. Systemic inflammation-derived proinflammatory cytokines/chemokines and other factors cause a breach in the blood brain-barrier (BBB) thereby allowing for the entry of immune/inflammatory cells including mast cell progenitors, mast cells and proinflammatory cytokines and chemokines into the brain. These peripheral-derived factors and intrinsically generated cytokines/chemokines, α-synuclein, corticotropin-releasing hormone (CRH), substance P (SP), beta amyloid 1–42 (Aβ1–42) peptide and amyloid precursor proteins can activate glial cells, T-cells and mast cells in the brain can induce additional release of inflammatory and neurotoxic molecules contributing to chronic neuroinflammation and neuronal death. The glia maturation factor (GMF), a proinflammatory protein discovered in our laboratory released from glia, activates mast cells to release inflammatory cytokines and chemokines. Chronic increase in the proinflammatory mediators induces neurotoxic Aβ and plaque formation in AD brains and neurodegeneration in PD brains. Glial cells, mast cells and T-cells can reactivate each other in neuroinflammatory conditions in the brain and augment neuroinflammation. Further, inflammatory mediators from the brain can also enter into the peripheral system through defective BBB, recruit immune cells into the brain, and exacerbate neuroinflammation. We suggest that mast cell-associated inflammatory mediators from systemic inflammation and brain could augment neuroinflammation and neurodegeneration in the brain. This review article addresses the role of some atypical inflammatory mediators that are associated with mast cell inflammation and their activation of glial cells to induce neurodegeneration.

show abstract

Section: Neuropeptides Sp and Crh In Neuroinflammationmentioning

confidence: 99%

Brain and Peripheral Atypical Inflammatory Mediators Potentiate Neuroinflammation and Neurodegeneration

Kempuraj

Thangavel

Selvakumar

et al. 2017

Front. Cell. Neurosci.

359

265

View full text Add to dashboard Cite

show abstract

“…As a neurotransmitter or neuromodulator, it plays an important role in the nervous system. Neurokinin 1 (NK1) receptor is the specific receptor for SP (19,20). Exogenous SP can stimulate the proliferation and differentiation of fibroblasts on the wound surface, accelerate synthesis and secretion of angiogenesis factors and collagen fibers, and play a significant role in wound healing and scar hyperplasia (21).…”

Section: Introductionmentioning

confidence: 99%

Nerve growth factor and substance P may be involved in moist exposed burn ointment‑mediated chronic refractory wound healing

Wang

et al. 2018

Exp Ther Med

View full text Add to dashboard Cite

Moist exposed burn ointment (MEBO) is becoming increasingly popular in China as it shortens wound-healing time and reduces scar formation. However, its exact mechanism in mediating the wound-healing process is not yet clear. In the present study a total of 90 healthy adult male Wistar rats of specific-pathogen-free grade were divided equally into a control group, wound group, MEBO group, recombinant bovine basic fibroblast growth factor (rb-bFGF) group and sham operation group. Wound healing was observed from the extracted granulation tissues and recorded at three time points on 3, 7 and 14 days. Different levels of tumor necrosis factor α (TNF-α) and interleukin-6 (IL-6) in tissue homogenate were detected using ELISA. Western blot analysis and quantitative PCR were used to detect the expression of nerve growth factor (NGF), substance P (SP) as well as tyrosine kinase A (TrkA) receptor protein and the corresponding mRNA levels in granulation tissue. It was observed that the wound healing progressed faster in the MEBO and rb-bFGF groups compared with the wound group (P<0.01). TNF-α and IL-6 had an upward-downward trend at three time points, with the wound group demonstrating the most obvious increase (P<0.01). NGF and SP mRNA and protein levels in granulation tissue in MEBO, rb-bFGF and sham operation groups reached their highest levels on day 7 and then decreased on day 14. The expression level of TrkA was also measured simultaneously and its expression pattern was similar to that of NGF and SP. These results suggested that MEBO may promote nerve repair and accelerate wound healing through mediating the expression levels of NGF and SP, as well as TrkA.

show abstract

“…It is well known that the activation of NK1 by Substance P (SP) regulates the stress response and induces anxiety-like behavior and that NK 1 R antagonists have anxiolytic-like properties (Santarelli et al, 2001; Ebner and Singewald, 2006; Ebner et al, 2008). The PVN receives substance P innervation, and NK 1 R stimulation activates the HPA axis, enhancing corticosterone release and the expression of CRF1R (Kawano and Masuko, 1992; Hamke et al, 2006; Mello et al, 2007; Womack and Barrett-Jolley, 2007; Womack et al, 2007; Ebner et al, 2008). On the other hand, it was also reported that NK antagonist administration can increase adrenocorticotropic hormone (ACTH) release and CRF expression (Jessop et al, 2000) and that SP can suppress ACTH release (Jones et al, 1978)r. These effects of NK1R antagonists, however, occur in unstressed animals, and therefore, they suggest a tonic suppression of HPA axis activity by SP/NK1R.…”

Section: Nk1 Receptormentioning

confidence: 99%

Emerging targets for addiction neuropharmacology

Ubaldi

Cannella

Ciccocioppo

2016

Progress in Brain Research

View full text Add to dashboard Cite

Drug abuse represents a considerable burden of disease and has enormous economic impacts on societies. Over the years, few medications have been developed for clinical use. Their utilization is endowed with several limitations, including partial efficacy or significant side effects. On the other hand, the successful advancement of these compounds provides an important proof-of-concept for the feasibility of drug development programs in addiction. In recent years, a wealth of information has been generated on the psychological mechanisms, genetic or epigenetic predisposing factors, and neurobiological adaptations induced by drug consumption that interact with each other to contribute to disease progression. It is now clear that addiction develops through phases, from initial recreational use to excessive consumption and compulsive drug seeking, with a shift from positive to negative reinforcement driving motivated behaviors. A greater understanding of these mechanisms has opened new vistas in drug development programs. Researchers’ attention has been shifted from investigation of classical targets associated with reward to biological substrates responsible for negative reinforcement, impulse loss of control and maladaptive mechanisms resulting from protracted drug use. From this research, several new biological targets for the development of innovative therapies have started to emerge. The present article offers an overview of targets currently under scrutiny for the development of new medications for addiction. This work is not exhaustive but rather it provides a few examples of how this research has advanced in recent years by virtue of studies carried out in our laboratory.

show abstract

Substance P induces expression of the corticotropin-releasing factor receptor 1 by activation of the neurokinin-1 receptor

Cited by 26 publications

References 54 publications

Brain and Peripheral Atypical Inflammatory Mediators Potentiate Neuroinflammation and Neurodegeneration

Brain and Peripheral Atypical Inflammatory Mediators Potentiate Neuroinflammation and Neurodegeneration

Nerve growth factor and substance P may be involved in moist exposed burn ointment‑mediated chronic refractory wound healing

Emerging targets for addiction neuropharmacology

Contact Info

Product

Resources

About