Transmembrane protein TMEM184B is necessary for interleukin-31–induced itch

Larsen, Erik G.; Cho, Tiffany S.; McBride, Matthew L.; Feng, Jing; Manivannan, Bhagyashree; Madura, Cynthia L.; Klein, Nathaniel; Wright, Elizabeth B.; Wickstead, E.; Garcia‐Verdugo, Hector D.; Khanna, Rajesh; Hu, Hongzhen; Bhattacharya, Martha R.C.

doi:10.1097/j.pain.0000000000002452

Cited by 9 publications

(16 citation statements)

References 34 publications

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“…To evaluate common signatures of TMEM184B-dependent gene expression across disparate types of neurons, we compared the differentially expressed genes (Adjusted p < 0.05) between our 5 month hippocampus data set and one we have previously reported from 6 month adult dorsal root ganglia [10]. Among differentially expressed genes, we identified 12 genes (including Tmem184b itself) that were similarly regulated (Figure 5 and Additional File 8).…”

Section: Resultsmentioning

confidence: 99%

Transmembrane protein 184B (TMEM184B) promotes expression of synaptic gene networks in the mouse hippocampus

Larsen¹,

Wright²,

Hart³

et al. 2022

Preprint

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In Alzheimer’s Disease (AD) and other dementias, hippocampal synaptic dysfunction and loss contribute to the progression of memory impairment. Recent analysis of human AD transcriptomes has provided a list of gene candidates that may serve as drivers of disease. One such candidate is the membrane protein TMEM184B. To evaluate whether TMEM184B contributes to neurological impairment, we asked whether loss of TMEM184B in mice causes gene expression or behavior alterations, focusing on the hippocampus. Because one major risk factor for AD is age, we compared young adult (5-month-old) and aged (15-month-old) wild type and Tmem184b-mutant mice to assess the dual contributions of age and genotype. TMEM184B loss altered expression of pre- and post-synaptic transcripts by 5 months and continued through 15 months, specifically affecting genes involved in synapse assembly and neural development. Wnt-activated enhancer elements were enriched among differentially expressed genes, suggesting an intersection with this pathway. Few differences existed between young adult and aged mutants, suggesting that transcriptional effects of TMEM184B loss are relatively constant. To understand how TMEM184B disruption may impact behaviors, we evaluated memory using the novel object recognition test and anxiety using the elevated plus maze. Young adult Tmem184b-mutant mice show normal object discrimination, suggesting a lack of memory impairment at this age. However, mutant mice showed decreased anxiety, a phenotype seen in neurodevelopmental disorders. Taken together, our data suggest that TMEM184B is required for proper synaptic gene expression and function but may not be causal for AD and related dementias.

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Section: Resultsmentioning

confidence: 99%

Transmembrane protein 184B (TMEM184B) promotes expression of synaptic gene networks in the mouse hippocampus

Larsen¹,

Wright²,

Hart³

et al. 2022

Preprint

Self Cite

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“…Bhattacharya et al 22 found that TMEM184B is highly expressed in the nervous system with axon degeneration and neuromuscular junction maintenance in mice, suggesting that TMEM184B strongly influences the regulation of axonal degeneration and peripheral nervous system morphology and function. Larsen et al 23 found that TMEM184B promoted adult somatosensation through developmental Wnt signalling pathway. Rasmussen et al 24 noted that TMEM184B might regulate ibuprofen uptake by type I cells of Madin‐Darby canine kidneys (MDCK) under hyperosmotic conditions and was regulated by the transcription factor Nfat5.…”

Section: Discussionmentioning

confidence: 99%

“…18,19 Previous studies have confirmed that several proteins in the TMEM family are abnormally found that TMEM184B is highly expressed in the nervous system with axon degeneration and neuromuscular junction maintenance in mice, suggesting that TMEM184B strongly influences the regulation of axonal degeneration and peripheral nervous system morphology and function. Larsen et al 23…”

Section: Discussionmentioning

confidence: 99%

TMEM184B promotes proliferation, migration and invasion, and inhibits apoptosis in hypopharyngeal squamous cell carcinoma

Lin

Liu

et al. 2022

J Cellular Molecular Medi

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Hypopharyngeal squamous cell carcinoma (HPSCC) accounts for approximately 3% of all head and neck squamous cell carcinoma (HNSCC). The incidence of HPSCC has increased during the past three decades. 1,2 Although HPSCC is relatively uncommon, it is one of aggressive and lethal forms among HNSCCs. HPSCC is characterized by its wide submucosal spread, early lymph node metastasis, distal metastasis and diagnosis with a later stage. Although improvements have been made to treatments, such as surgery, radiotherapy, chemotherapy, immunotherapy and in their combination in recent decades, 3,4 the 5 years overall survival of HPSCC remains approximately 30%-35%. 5 As hypopharynx is anatomically adjacent to the larynx, the advancedstage HPSCC may severely impair the structure and function of the

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“…In addition, cutaneous and intrathecal injections of IL-31 evoked intense itch, which was TRPV1 and TRPA1-dependent [113]. Moreover, a more recent study showed that transmembrane protein 184B (TMEM184B) is necessary for IL-31-induced itch [116]. Thus, the details of the mechanism of IL-31-induced itch are becoming clearer, and target molecules that can lead to treatment are being identified one after another.…”

Section: Il-31mentioning

confidence: 99%

Connections between Immune-Derived Mediators and Sensory Nerves for Itch Sensation

Toyama

Tominaga

Takamori

2021

IJMS

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Although histamine is a well-known itch mediator, histamine H1-receptor blockers often lack efficacy in chronic itch. Recent molecular and cellular based studies have shown that non-histaminergic mediators, such as proteases, neuropeptides and cytokines, along with their cognate receptors, are involved in evocation and modulation of itch sensation. Many of these molecules are produced and secreted by immune cells, which act on sensory nerve fibers distributed in the skin to cause itching and sensitization. This understanding of the connections between immune cell-derived mediators and sensory nerve fibers has led to the development of new treatments for itch. This review summarizes current knowledge of immune cell-derived itch mediators and neuronal response mechanisms, and discusses therapeutic agents that target these systems.

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Transmembrane protein TMEM184B is necessary for interleukin-31–induced itch

Abstract: Supplemental Digital Content is Available in the Text.Transmembrane protein 184B is necessary for the proper function of itch-sensitive sensory neurons involved in eczema through the control of Wnt pathway gene expression during development.

Cited by 9 publications

References 34 publications

Transmembrane protein 184B (TMEM184B) promotes expression of synaptic gene networks in the mouse hippocampus

Transmembrane protein 184B (TMEM184B) promotes expression of synaptic gene networks in the mouse hippocampus

TMEM184B promotes proliferation, migration and invasion, and inhibits apoptosis in hypopharyngeal squamous cell carcinoma

Connections between Immune-Derived Mediators and Sensory Nerves for Itch Sensation

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