Inactive AT1 angiotensin receptor acts as a signaling hub: a novel mechanism of receptor cross-talk

16,16-Dimethyl-PGE2 (PGE2) may interact with one of four prostaglandin type E (EP) receptors, which signal via cAMP (via EP2 or EP4 receptors) or intracellular Ca2+ (via EP1 receptors). Furthermore, EP3 receptors have several splice variants, which may signal via cAMP or intracellular Ca2+. We sought to determine the PGE2 receptor interactions that mediate recovery of transmucosal resistance ( R) in ischemia-injured porcine ileum. Porcine ileum was subjected to 45 min of ischemia, after which the mucosa was mounted in Ussing chambers. Tissues were pretreated with indomethacin (5 μM). Treatment with the EP1, EP2, EP3, and EP4 agonist PGE2 (1 μM) elevated R twofold and significantly increased tissue cAMP content, whereas the EP2 and EP4 agonist deoxy-PGE1 (1 μM) or the EP1 and EP3 agonist sulprostone (1 μM) had no effect. However, a combination of deoxy-PGE1 and sulprostone stimulated synergistic elevations in R and tissue cAMP content. Furthermore, treatment of tissues with deoxy-PGE1 and the Ca2+ ionophore A-23187 stimulated synergistic increases in R and cAMP, indicating that PGE2 triggers recovery of R via EP receptor cross talk mechanisms involving cAMP and intracellular Ca2+.

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Thyroid stimulating hormone (TSH)/insulin-like growth factor 1 (IGF1) receptor cross-talk in Human cells

Current Opinion in Endocrine and Metabolic Research ◽

10.1016/j.coemr.2018.01.007 ◽

2018 ◽

Vol 2 ◽

pp. 29-33 ◽

Cited By ~ 3

Author(s):

Christine C. Krieger ◽

Sarah J. Morgan ◽

Susanne Neumann ◽

Marvin C. Gershengorn

Keyword(s):

Growth Factor ◽

Cross Talk ◽

Thyroid Stimulating Hormone ◽

Human Cells ◽

Insulin Like Growth Factor ◽

Igf1 Receptor ◽

Receptor Cross Talk ◽

Stimulating Hormone

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Retinoid Receptor Cross-Talk

Encyclopedia of Cancer ◽

10.1007/978-3-662-46875-3_5073 ◽

2016 ◽

pp. 4059-4062

Author(s):

Athanasios G. Papavassiliou ◽

Michalis V. Karamouzis

Keyword(s):

Cross Talk ◽

Retinoid Receptor ◽

Receptor Cross Talk

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Receptor Cross-Talk

Encyclopedia of Cancer ◽

10.1007/978-3-642-27841-9_4976-3 ◽

2017 ◽

pp. 1-6

Author(s):

Steven A. Rosenzweig ◽

David M. Neskey

Keyword(s):

Cross Talk ◽

Receptor Cross Talk

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A Fish Leukocyte Immune-Type Receptor Uses a Novel Intracytoplasmic Tail Networking Mechanism to Cross-Inhibit the Phagocytic Response

International Journal of Molecular Sciences ◽

10.3390/ijms21145146 ◽

2020 ◽

Vol 21 (14) ◽

pp. 5146

Author(s):

Chenjie Fei ◽

Myron A. Zwozdesky ◽

James L. Stafford

Keyword(s):

Cross Talk ◽

Ictalurus Punctatus ◽

Immune Cell ◽

Integrated Control ◽

Immunoglobulin Superfamily ◽

Functional Assessments ◽

Inhibitory Signaling ◽

Receptor Cross Talk ◽

Cross Inhibition ◽

Phagocytic Response

Channel catfish (Ictalurus punctatus) leukocyte immune-type receptors (IpLITRs) are a family of immunoregulatory proteins shown to regulate several innate immune cell effector responses, including phagocytosis. The precise mechanisms of IpLITR-mediated regulation of the phagocytic process are not entirely understood, but we have previously shown that different IpLITR-types use classical as well as novel pathways for controlling immune cell-mediated target engulfment. To date, all functional assessments of IpLITR-mediated regulatory actions have focused on the independent characterization of select IpLITR-types in transfected cells. As members of the immunoglobulin superfamily, many IpLITRs share similar extracellular Ig-like domains, thus it is possible that various IpLITR actions are influenced by cross-talk mechanisms between different IpLITR-types; analogous to the paired innate receptor paradigm in mammals. Here, we describe in detail the co-expression of different IpLITR-types in the human embryonic AD293 cell line and examination of their receptor cross-talk mechanisms during the regulation of the phagocytic response using imaging flow cytometry, confocal microscopy, and immunoprecipitation protocols. Overall, our data provides interesting new insights into the integrated control of phagocytosis via the antagonistic networking of independent IpLITR-types that requires the selective recruitment of inhibitory signaling molecules for the initiation and sustained cross-inhibition of phagocytosis.

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