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Related Concept Videos

Enzyme-linked Receptors01:00

Enzyme-linked Receptors

Enzyme-linked receptors are proteins that act as both receptor and enzyme, activating multiple intracellular signals. This is a large group of receptors that include the receptor tyrosine kinase (RTK) family. Many growth factors and hormones bind to and activate the RTKs.
Neurotrophin (NT) receptors are a family of RTKs, including trkA, trkB, and trkC (tropomyosin-related kinase) receptors. TrkA is specific for nerve growth factor (NGF), neurotrophin-6, and neurotrophin-7. TrkB binds...
Receptor Tyrosine Kinases01:26

Receptor Tyrosine Kinases

Receptor tyrosine kinases or RTKs are membrane-bound receptors that phosphorylate specific tyrosine on protein substrates. RTKs regulate cellular growth, differentiation, survival, and migration. They contain an extracellular ligand binding domain, a transmembrane domain, and a cytosolic tail with intrinsic kinase activity. Several extracellular signaling molecules activate RTKs in one or more ways and relay the signal downstream. Ligands such as platelet-derived growth factor (PDGF) or...
GPCR Desensitization01:12

GPCR Desensitization

G protein-coupled receptor (GPCR) signaling plays a crucial role in cell functioning. GPCR desensitization is an equally essential process. It allows cells to respond to changing environments and regain sensitivity to new stimuli while preventing unnecessary stimulation when no longer needed. Prolonged exposure to stimuli leads to GPCR desensitization. It involves blocking the receptors from binding and activating additional G proteins. This inhibits activation of downstream effectors, thereby...
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a rapamycin-insensitive companion...

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Related Experiment Videos

TRPC channel-mediated neuroprotection by PDGF involves Pyk2/ERK/CREB pathway.

H Yao1, F Peng, Y Fan

  • 1Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, NE 68198-5880, USA.

Cell Death and Differentiation
|August 15, 2009
PubMed
Summary

Platelet-derived growth factor-BB (PDGF) protects dopaminergic neurons from HIV-1 Tat toxicity. This neuroprotection involves transient receptor potential canonical (TRPC) channels and is confirmed in mouse models of HIV-associated dementia.

Related Experiment Videos

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Cell Biology

Background:

  • Platelet-derived growth factor-BB (PDGF) supports central nervous system neurons.
  • The role of PDGF in protecting dopaminergic neurons, particularly in HIV-associated dementia (HAD), is not well understood.

Purpose of the Study:

  • To investigate the neuroprotective effects of PDGF against HIV-1 Tat toxicity in dopaminergic neurons.
  • To elucidate the involvement of transient receptor potential canonical (TRPC) channels in PDGF-mediated neuroprotection.

Main Methods:

  • Primary midbrain neuron cultures were used to assess PDGF's neuroprotective effects against HIV-1 Tat.
  • TRPC channel function was blocked using pharmacological inhibitors and short-interfering RNAs (siRNAs) targeting TRPC 5 and 6.
  • Intracellular calcium (Ca2+) levels and signaling pathways (ERK/CREB, PI3K/Akt) were analyzed.
  • In vivo studies involved intrastriatal injections of PDGF and HIV-1 Tat in mice.

Main Results:

  • Exogenous PDGF demonstrated neuroprotection against HIV-1 Tat-induced toxicity in primary neurons.
  • Blocking TRPC channels abrogated PDGF-mediated neuroprotection and reduced intracellular Ca2+ influx.
  • PDGF-induced neuroprotection involved both ERK/CREB and PI3K/Akt pathways, with TRPC channel blockade affecting Pyk2/ERK/CREB activation.
  • In vivo, PDGF administration rescued dopaminergic neurons from Tat-induced neurotoxicity in mice, an effect diminished by TRP channel blockers.

Conclusions:

  • PDGF confers neuroprotection to dopaminergic neurons against HIV-1 Tat toxicity.
  • TRPC channels play a crucial role in mediating PDGF's neuroprotective effects.
  • These findings highlight TRPC channels as potential therapeutic targets for neuroprotection in conditions like HAD.