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Related Concept Videos

Sympathetic Signaling01:31

Sympathetic Signaling

Sympathetic signaling, a vital part of the autonomic nervous system, plays a crucial role in mobilizing the body's resources in response to stress or emergencies. It involves the transmission of nerve impulses from sympathetic preganglionic fibers to postganglionic fibers. This results in the release of specific neurotransmitters and activation of adrenergic receptors.
Sympathetic preganglionic fibers release the neurotransmitter acetylcholine (ACh) onto the ganglionic neurons in the...
Transducer Mechanism: Enzyme-Linked Receptors01:27

Transducer Mechanism: Enzyme-Linked Receptors

Enzyme-linked receptors are cell-surface receptors acting as an enzyme or associating with an enzyme intracellularly. They make excellent drug targets. Drugs can bind to the extracellular ligand-binding domain or directly affect their enzymatic domain and alter their activity.
Major types that are helpful drug targets include:
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...
Amplifying Signals via Enzymatic Cascade01:22

Amplifying Signals via Enzymatic Cascade

When a ligand binds to a cell-surface receptor, the receptor's intracellular domain changes shape, which may either activate its enzyme function or allow its binding to other molecules. The initial signal is amplified by most signal transduction pathways. This means that a single ligand molecule can activate multiple molecules of a downstream target. Proteins that relay a signal are most commonly phosphorylated at one or more sites, activating or inactivating the protein. Kinases catalyze the...
Endocrine Signaling01:45

Endocrine Signaling

Endocrine cells produce hormones to communicate with remote target cells found in other organs. The hormone reaches these distant areas using the circulatory system. This exposes the whole organism to the hormone but only those cells expressing hormone receptors or target cells are affected. Thus, endocrine signaling induces slow responses from its target cells but these effects also last longer.
Parasympathetic Signaling01:30

Parasympathetic Signaling

Parasympathetic signaling plays a crucial role in regulating various physiological processes. It involves the release of acetylcholine (ACh) by parasympathetic neurons, which can have localized and short-lived effects. The majority of ACh released is rapidly inactivated at the synapse by the enzyme acetylcholinesterase (AChE), which hydrolyzes Ach into choline and acetate. Additionally, the tissue cholinesterase deactivates any ACh diffusing into the surrounding tissues.
The effects of...

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Related Experiment Videos

A signaling network in phenylephrine-induced benign prostatic hyperplasia.

Jayoung Kim1, Yutaka Yanagihara, Tadahiko Kikugawa

  • 1Departments of Surgery andBiological Chemistry and Molecular Pharmacology, Harvard Medical School, The Urological Diseases Research Center, Children's Hospital, Boston, Massachusetts 02115, USA. michael.freeman@childrens.harvard.edu

Endocrinology
|May 16, 2009
PubMed
Summary

Researchers identified molecular mechanisms of benign prostatic hyperplasia (BPH) using a rat model. They found inflammatory pathways and clusterin (apolipoprotein J) are key, suggesting clusterin as a potential therapeutic target for BPH.

Related Experiment Videos

Area of Science:

  • Urology
  • Molecular Biology
  • Bioinformatics

Background:

  • Benign prostatic hyperplasia (BPH) is an age-related condition causing prostate enlargement.
  • The exact molecular mechanisms driving BPH development remain largely unknown.
  • Existing research lacks comprehensive molecular network models for BPH.

Purpose of the Study:

  • To elucidate the molecular underpinnings of BPH development.
  • To construct a molecular network model for adrenergic-induced BPH.
  • To identify novel therapeutic targets for BPH.

Main Methods:

  • Utilized a rat model with chronic alpha(1)-adrenergic stimulation (phenylephrine) to mimic human BPH.
  • Performed DNA microarray analysis on prostate tissue.
  • Applied bioinformatic tools to build a signal transduction pathway network.
  • Independently validated key findings, including TGF-beta signaling and clusterin expression.

Main Results:

  • Identified significant involvement of inflammatory pathways in BPH development.
  • Revealed activation of a transforming growth factor-beta (TGF-beta) signaling cascade.
  • Discovered clusterin (apolipoprotein J) as a prominent network node.
  • Confirmed clusterin's gene and protein expression and TGF-beta responsiveness.

Conclusions:

  • This study presents the first comprehensive molecular network for adrenergic-induced BPH.
  • Inflammatory pathways and TGF-beta signaling are crucial in BPH pathogenesis.
  • Clusterin (apolipoprotein J) emerges as a novel and promising biochemical target for BPH therapy.