cellular response to hydrogen sulfide

Definition

Target type: biologicalprocess

Any process that results in a change in state or activity of a cell (in terms of movement, secretion, enzyme production, gene expression, etc.) as a result of a hydrogen sulfide stimulus. [GO_REF:0000071, GOC:TermGenie, PMID:24012591]

Cellular response to hydrogen sulfide is a complex process involving multiple signaling pathways and cellular responses. Hydrogen sulfide (H2S) is a gaseous signaling molecule with diverse physiological and pathological roles. It acts as a modulator of various cellular processes, including inflammation, oxidative stress, apoptosis, and angiogenesis.

Upon exposure to H2S, cells initiate a cascade of events to counteract its effects and maintain homeostasis. This response can be broadly categorized into:

**1. Sensing and Signaling:**

* **H2S detection:** Cells detect H2S through specific receptors and enzymes, such as the cysteine-rich protein 61 (CYR61), the transient receptor potential ankyrin 1 (TRPA1) channel, and the sulfide quinone oxidoreductase (SQR) enzyme. These receptors and enzymes trigger downstream signaling pathways.

* **Signal transduction:** Upon H2S binding, these receptors activate various signaling cascades, including the mitogen-activated protein kinase (MAPK) pathway, the phosphatidylinositol 3-kinase (PI3K)/Akt pathway, and the nuclear factor kappa B (NF-κB) pathway.

**2. Cellular Responses:**

* **Antioxidant defense:** H2S acts as an antioxidant by directly scavenging reactive oxygen species (ROS) and inducing the expression of antioxidant enzymes like superoxide dismutase (SOD) and glutathione peroxidase (GPx). This reduces oxidative stress and protects cells from damage.

* **Inflammation modulation:** H2S plays a role in both pro- and anti-inflammatory responses depending on the context. It can suppress inflammation by inhibiting NF-κB activation and reducing the production of pro-inflammatory cytokines like TNF-α and IL-6. However, in certain situations, H2S can also promote inflammation.

* **Apoptosis regulation:** H2S has been shown to both induce and inhibit apoptosis, depending on the cell type, concentration, and exposure time. It can activate caspase-dependent apoptotic pathways and promote cell death under certain conditions. Conversely, it can also protect cells from apoptosis by suppressing ROS production and activating survival pathways.

* **Angiogenesis regulation:** H2S can stimulate angiogenesis (formation of new blood vessels) by promoting the migration and proliferation of endothelial cells. It achieves this by activating the PI3K/Akt pathway and increasing the production of vascular endothelial growth factor (VEGF).

* **Other cellular processes:** H2S also influences various other cellular processes, such as energy metabolism, cell cycle regulation, and neurotransmission.

**3. Cellular Adaptation and Homeostasis:**

* **Long-term adaptation:** Cells can adapt to chronic H2S exposure by modulating the expression of H2S-metabolizing enzymes and receptors. This fine-tunes the cellular response and maintains homeostasis.

* **Cellular adaptation:** Prolonged exposure to H2S can lead to cellular adaptation, where cells become less sensitive to the effects of H2S. This is often observed in conditions of chronic H2S exposure, such as in individuals with chronic obstructive pulmonary disease (COPD).

In conclusion, cellular response to hydrogen sulfide is a highly dynamic and multifaceted process that involves various signaling pathways and cellular responses. This intricate regulation ensures that cells can properly respond to this critical gaseous signaling molecule and maintain homeostasis in the face of environmental stressors.'
"

Proteins (1)

Compounds (220)