Substance P Activates Both Contractile and Inflammatory Pathways in Lymphatics Through the Neurokinin Receptors NK1R and NK3R

Chakraborty, Sanjukta; Nepiyushchikh, Zhanna; Davis, Michael J.; Zawieja, David C.; Muthuchamy, Mariappan

doi:10.1111/j.1549-8719.2010.00064.x

Cited by 36 publications

(29 citation statements)

References 53 publications

(98 reference statements)

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“…Western blot analysis was carried out as previously described (7). Briefly, LECs were directly lysed using 1ϫ SDS buffer, and proteins were separated on a 4 -20% SDS-polyacrylamide gel.…”

Section: Methodsmentioning

confidence: 99%

MicroRNA signature of inflamed lymphatic endothelium and role of miR-9 in lymphangiogenesis and inflammation

Chakraborty

Zawieja

Davis

et al. 2015

American Journal of Physiology-Cell Physiology

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Chakraborty S, Zawieja DC, Davis MJ, Muthuchamy M. MicroRNA signature of inflamed lymphatic endothelium and role of miR-9 in lymphangiogenesis and inflammation. Am J Physiol Cell Physiol 309: C680 -C692, 2015. First published September 9, 2015; doi:10.1152/ajpcell.00122.2015.-The lymphatics have emerged as critical players in the progression and resolution of inflammation. The goal of this study was to identify specific microRNAs (miRNAs) that regulate lymphatic inflammatory processes. Rat mesenteric lymphatic endothelial cells (LECs) were exposed to the proinflammatory cytokine tumor necrosis factor-␣ for 2, 24, and 96 h, and miRNA profiling was carried out by real-time PCR arrays. Our data demonstrate a specific set of miRNAs that are differentially expressed (Ͼ1.8-fold and/or P Ͻ 0.05) in LECs in response to tumor necrosis factor-␣ and are involved in inflammation, angiogenesis, endothelial-mesenchymal transition, and cell proliferation and senescence. We further characterized the expression of miRNA 9 (miR-9) that was induced in LECs and in inflamed rat mesenteric lymphatics. Our results showed that miR-9 overexpression significantly repressed NF-B expression and, thereby, suppressed inflammation but promoted LEC tube formation, as well as expression of the prolymphangiogenic molecules endothelial nitric oxide synthase and VEGF receptor type 3. LEC viability and proliferation and endothelial-mesenchymal transition were also significantly induced by miR-9. This study provides the first evidence of a distinct profile of miRNAs associated with LECs during inflammation. It also identifies the critical dual role of miR-9 in fine-tuning the balance between lymphatic inflammatory and lymphangiogenic pathways.

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“…Western blot analysis was carried out as previously described (7). Briefly, LECs were directly lysed using 1ϫ SDS buffer, and proteins were separated on a 4 -20% SDS-polyacrylamide gel.…”

Section: Methodsmentioning

confidence: 99%

MicroRNA signature of inflamed lymphatic endothelium and role of miR-9 in lymphangiogenesis and inflammation

Chakraborty

Zawieja

Davis

et al. 2015

American Journal of Physiology-Cell Physiology

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“…Lymphatic vessels mediate lipid absorption and transportation, share an intimate spatial association with adipose tissue, and regulate the traffic of immune cells, 210,211 whereas neuropeptides, such as substance-P (SP), have substantial effects on lymphatic functions, creating lymphatic function and inflammation. 212,213 Lymph stasis and/or fluid leakage from lymphatic vessels can promote fat accumulation. 214 When intestinal lymphatic drainage is interrupted, an obvious increase in MAT deposition gradually develops.…”

Section: Cross Talk Between Mesenteric Tissuesmentioning

confidence: 99%

The Role of the Mesentery in Crohnʼs Disease

Zhu

Zuo

et al. 2016

Inflammatory Bowel Diseases

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Crohn's disease (CD) is a complex gastrointestinal disorder involving multiple levels of cross talk between the immunological, neural, vascular, and endocrine systems. The current dominant theory in CD is based on the unidirectional axis of dysbiosis-innate immunity-adaptive immunity-mesentery-body system. Emerging clinical evidence strongly suggests that the axis be bidirectional. The morphologic and/or functional abnormalities in the mesenteric structures likely contribute to the disease progression of CD, to a less extent the disease initiation. In addition to adipocytes, mesentery contains nerves, blood vessels, lymphatics, stromal cells, and fibroblasts. By the secretion of adipokines that have endocrine functions, the mesenteric fat tissue exerts its activity in immunomodulation mainly through response to afferent signals, neuropeptides, and functional cytokines. Mesenteric nerves are involved in the pathogenesis and prognosis of CD mainly through neuropeptides. In addition to angiogenesis observed in CD, lymphatic obstruction, remodeling, and impaired contraction maybe a cause and consequence of CD. Lymphangiogenesis and angiogenesis play a concomitant role in the progress of chronic intestinal inflammation. Finally, the interaction between neuropeptides, adipokines, and vascular and lymphatic endothelia leads to adipose tissue remodeling, which makes the mesentery an active participator, not a bystander, in the disease initiation and precipitation CD. The identification of the role of mesentery, including the structure and function of mesenteric nerves, vessels, lymphatics, and fat, in the intestinal inflammation in CD has important implications in understanding its pathogenesis and clinical management.

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“…Nociceptor nerve fibers are also closely associated with lymphatic vessels. Substance P stimulates lymphatic vessel contractility and increases pump efficiency through its receptors TACR1 and TACR3 expressed by lymphatic smooth muscle cells [68,69]. CGRP increases constriction frequency of perfused lymphatic vessels, a phenomenon that is dependent on nitric oxide [70].…”

Section: Nociceptor Neuron Regulation Of Inflammation and Immunitymentioning

confidence: 99%

Nociceptor Sensory Neuron–Immune Interactions in Pain and Inflammation

Pinho‐Ribeiro

Verri

Chiu

2017

Trends in Immunology

707

626

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Nociceptor sensory neurons protect organisms from dangers by eliciting pain and driving avoidance. Pain also accompanies many types of inflammation and injury. It is increasingly clear that active crosstalk occurs between nociceptor neurons and the immune system to regulate pain, host defense, and inflammatory diseases. Immune cells at peripheral nerve terminals and within the spinal cord release mediators that modulate mechanical and thermal sensitivity. In turn, nociceptor neurons release neuropeptides and neurotransmitters from nerve terminals that regulate vascular, innate, and adaptive immune cell responses. Therefore, the dialogue between nociceptor neurons and the immune system is a fundamental aspect of inflammation, both acute and chronic. A better understanding of these interactions could produce approaches to treat chronic pain and inflammatory diseases.

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Substance P Activates Both Contractile and Inflammatory Pathways in Lymphatics Through the Neurokinin Receptors NK1R and NK3R

Cited by 36 publications

References 53 publications

MicroRNA signature of inflamed lymphatic endothelium and role of miR-9 in lymphangiogenesis and inflammation

MicroRNA signature of inflamed lymphatic endothelium and role of miR-9 in lymphangiogenesis and inflammation

The Role of the Mesentery in Crohnʼs Disease

Nociceptor Sensory Neuron–Immune Interactions in Pain and Inflammation

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