IndraLab

Statements



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"Moreover, selective genetic deletion of BDNF in Nav1.8 positive sensory neurons also reduced inflammation without influencing neuropathic sensitivity (Zhao et al., 2006)."

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"Riol-Blanco et al. showed in this model that TRPV1 + Nav 1.8 + neurons are essential drivers of this inflammatory response, through promotion of an IL-23/IL-17 pathway initiated by dermal DC activatio[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"However, we found that SNs caused some inflammation to the skin of the mice at the injection sites after hypodermic administration at 24 h and 7 days post-injection, as observed from histopathological[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"This finding suggests that Nav1.8 in epidermal keratinocytes may initiate inflammation and the development of rosacea and psoriasis.Impaired inflammatory signals in keratinocytes are essential for driving skin inflammation in rosacea and psoriasis [5,43]."

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"The addition of mtROS scavenger significantly reduced Nav1.8-C-induced upregulation of pro-inflammatory factors in keratinocytes, indicating that Nav1.8 promoted skin inflammation by driving ROS-mediated inflammatory signaling in keratinocytes."

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"First, as shown in Fig. 1C, mouse SNs were stimulated by a pro-inflammatory cytokine, TNF-α, to induce neuronal inflammation."

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"To reveal the potential mechanism by which Nav1.8 promotes skin inflammation, we performed RNAseq to identify genes that were abnormally expressed in rosacea-like skin lesions and regulated by Nav1.8."

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"In murine asthmatic lung inflammation, TRPA1 and Nav1.8 sensory neurons regulate the leukocyte infiltration (especially eosinophils) to the lungs and promoted allergen-induced airway inflammation and hyperreactivity (31, 64)."

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"Additionally, conditional knockout of Jak1 in NAV1.8 + neurons limited lung inflammation caused by ALT and the protease allergen papain 89 ( Figure 3 B)."