Endocrine cross‐talk between the gut microbiome and glial cells in development and disease

Anbalagan, Savani

doi:10.1111/jne.12924

Cited by 8 publications

(4 citation statements)

References 70 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Indeed, experimental evidence clearly indicates that dysbiosis occurs in several disorders characterized by myelin damage or disruption. Since shaping of the gut microbiota coincides with the critical period of developmental myelination, authors speculated on the regulation of the oligodendrocyte progenitor niche by the gut microbiota via different mechanisms (for review see [ 41 , 42 ]). Moreover, the absence of gut microbiota in GF mice reduced callosal myelination and white matter plasticity in the prefrontal cortex, due to reduced gene expression of myelin-related proteins and reduced levels of mature oligodendrocytes [ 43 ].…”

Section: Gut–glia Axis In Brain Physiology and Pathology: Modulation ...mentioning

confidence: 99%

Modulation of Glial Cell Functions by the Gut–Brain Axis: A Role in Neurodegenerative Disorders and Pain Transmission

Magni

Riboldi

Ceruti

2023

Cells

View full text Add to dashboard Cite

Studies on host microbiota and their interactions with the central nervous system (CNS) have grown considerably in the last decade. Indeed, it has been widely demonstrated that dysregulations of the bidirectional gut–brain crosstalk are involved in the development of several pathological conditions, including chronic pain. In addition, the activation of central and peripheral glial cells is also implicated in the pathogenesis and progression of pain and other neurodegenerative disorders. Recent preclinical findings suggest that the gut microbiota plays a pivotal role in regulating glial maturation, morphology and function, possibly through the action of different microbial metabolites, including the most studied short-chain fatty acids (SCFAs). Moreover, altered microbiota composition has been reported in CNS disorders characterized by glial cell activation. In this review, we discuss recent studies showing the role of the gut microbiota and the effects of its depletion in modulating the morphology and function of glial cells (microglia and astrocytes), and we hypothesize a possible role for glia–microbiota interactions in the development and maintenance of chronic pain.

show abstract

Section: Gut–glia Axis In Brain Physiology and Pathology: Modulation ...mentioning

confidence: 99%

Modulation of Glial Cell Functions by the Gut–Brain Axis: A Role in Neurodegenerative Disorders and Pain Transmission

Magni

Riboldi

Ceruti

2023

Cells

View full text Add to dashboard Cite

show abstract

“…Now, if we still argue that this is not classical endocrine signaling, and that we need a different name, then as I proposed previously, I suggest calling endocrine signaling via gasotransmitters 'gasocrine signaling'. 106 CONCLUSION With all the above listed arguments, I call oxygen and/or its derivatives a gasocrine signaling molecule acting via the receptor HIF1α or equivalent transcription factors on the organism. To ensure the survival of our ecosystem, we need appropriate model organisms and tools to study gasocrine signaling [107][108][109] .…”

Section: Is There a Receptor For Oxygen Or Not?mentioning

confidence: 99%

Arguments for gasocrine signaling

Anbalagan

2023

Preprint

View full text Add to dashboard Cite

In cellular signaling, a cell can send specific signals to another cell with a clear intention. The sent signals are sensed by the receiving cell, triggering a cellular response. If these sender and receiver cells are in direct physical proximity, the signaling is labeled as paracrine. If these cells are far and the signal is transported, the signaling is labeled as endocrine. In this manuscript, as others have argued in the past, I also argue that gasotransmitters must not be excluded as endocrine signaling molecules. I argue that, like LEGO bricks that can be built, dismantled, and rebuilt into anything of the builder's imagination, gasotransmitters are also LEGO bricks of endocrine signaling. I argue that we must bend the rules of definitions in endocrine signaling to incorporate gasotransmitter-based endocrine signaling, which I call gasocrine signaling. If the reason that oxygen is not considered an endocrine molecule is based on the fact that it does not satisfy the definition of signal – ‘signal is something that passes from a sender to a receiver that carries a ‘specific’ message’, then I argue that the ‘message’ is simply ‘live’ or ‘die’, depending on whether the organism is aerobe or anaerobe, respectively. I argue that HIFα is the receptor for oxygen. Gasocrine signaling, I propose, is our Earth’s equivalent of Na’vi’s connection with the ecosystem of Pandora in the movie Avatar.

show abstract

“…It has the potential to unite researchers in recognizing the importance of vertebrate animal model organisms whose gasocrine signaling is also influenced by diet, environment and non-host factors. [28][29][30][31][32][33][34][35][36] Finally, I propose a modification of the definition of 'gasocrine signaling' from 'a cell signaling event based on the binding of gaseous signaling molecules or gasotransmitters to gasoreceptor proteins' to 'a cell signaling event based on the interaction of gaseous signaling molecules or gasotransmitters to gasoreceptor proteins'. Accepting E. coli SoxR as a gasoreceptor will enable us to explore other transcription factor-based gasoreceptor proteins in the cells of almost all other organisms.…”

Section: Introductionmentioning

confidence: 99%

Redox state-dependent gasocrine signaling

Anbalagan

2024

Preprint

View full text Add to dashboard Cite

I recently proposed the term 'gasocrine signaling' to describe a cell signaling event based on the binding of gaseous signaling molecules or gasotransmitters to gasoreceptor proteins. To investigate gasocrine signaling, it is essential to identify all the gasoreceptors for the gases generated in a cell or that reach a cell. Proteins can undergo gas-dependent changes in redox states, regulating protein disulfide bond formation or cleavage. Protein disulfide bonds play a pivotal role in protein folding, stability, localization, cellular signaling, function and the evolution of life. Drawing an analogy with the wicket rule of Cricket, where a batsman is dismissed upon bail dislodgement, I propose that the redox states of proteins with signaling or transcriptional activities, dependent on gaseous signaling molecules or gasotransmitters, be termed simply as 'gasoreceptor activation states’. I propose E. coli SoxR is a gasoreceptor with transcriptional activities, while mammalian VEGFR2 kinase and CD36 fatty acid transporter represent other classes of gasoreceptors. Embracing the complexity and diversity of gasoreceptors will facilitate a systematic exploration of the almost infinite number of gasoreceptors and their role in gasocrine signaling. Finally, I propose a modification of the definition of 'gasocrine signaling' to ‘a cell signaling event based on the interaction of gaseous signaling molecules or gasotransmitters to gasoreceptor proteins’.

show abstract

Endocrine cross‐talk between the gut microbiome and glial cells in development and disease

Cited by 8 publications

References 70 publications

Modulation of Glial Cell Functions by the Gut–Brain Axis: A Role in Neurodegenerative Disorders and Pain Transmission

Modulation of Glial Cell Functions by the Gut–Brain Axis: A Role in Neurodegenerative Disorders and Pain Transmission

Arguments for gasocrine signaling

Redox state-dependent gasocrine signaling

Contact Info

Product

Resources

About