Related Experiment Video

Updated: May 7, 2026

Generation of an Immortalized Murine Brain Microvascular Endothelial Cell Line as an In Vitro Blood Brain Barrier Model
09:36

Generation of an Immortalized Murine Brain Microvascular Endothelial Cell Line as an In Vitro Blood Brain Barrier Model

Published on: August 29, 2012

18.9K

Medin induces pro-inflammatory activation of human brain vascular smooth muscle cells

Nina Karamanova1, Kaleb T Morrow1, Alana Maerivoet2

  • 1Phoenix Veterans Affairs Health Care System, Phoenix, Arizona, USA.

Physiological Reports
|June 12, 2025
PubMed

Insights

Medin protein accumulation in blood vessels with aging promotes inflammation in human brain vascular smooth muscle cells (VSMCs). Inhibiting nuclear factor-κB (NFκB) partially reduces this medin-induced inflammation, suggesting medin as a therapeutic target for vascular aging.

Area of Science:

  • Vascular Biology
  • Aging Research
  • Cellular Inflammation

Background:

  • Medin is an amyloidogenic protein that accumulates in vasculature with aging.
  • Vascular smooth muscle cell (VSMC) activation contributes to vascular aging pathology.

Purpose of the Study:

  • To investigate the effects of medin on human brain VSMC activation.
  • To determine the role of nuclear factor-κB (NFκB) in medin-induced VSMC pro-inflammatory responses.

Main Methods:

  • VSMCs were treated with medin (0.5, 1, 5 μM) with or without an NFκB inhibitor (RO106-9920).
  • Gene and protein expression/secretion of inflammatory factors (IL-6, IL-8, MCP-1) and VSMC markers (ACTA2, MYH11, NOX4) were quantified using PCR and ELISA/Western blot.

Main Results:

  • Medin significantly increased VSMC gene expression and protein secretion of IL-6, IL-8, and MCP-1.
  • NFκB inhibition partially reduced medin-induced IL-6 and IL-8 secretion, with a trend for MCP-1.
  • Medin did not alter the expression of ACTA2, MYH11, or NOX4, indicating no effect on VSMC phenotypic transformation.

Conclusions:

  • Medin induces pro-inflammatory activation of human brain VSMCs.
  • This activation is partially mediated by the NFκB pathway.
  • Medin is a potential therapeutic target for mitigating vascular aging pathology.
Keywords:
agingamyloidinflammationsmooth muscle dysfunctionvascular dementia

More Related Videos

Neisseria meningitidis Infection of Induced Pluripotent Stem-Cell Derived Brain Endothelial Cells10:12

Neisseria meningitidis Infection of Induced Pluripotent Stem-Cell Derived Brain Endothelial Cells

Published on: July 14, 2020

2.3K
Author Spotlight: Insight Into Advances in Prion Diseases Research10:40

Author Spotlight: Insight Into Advances in Prion Diseases Research

Published on: August 11, 2023

436

Related Concept Videos

Antihypertensive Drugs: Vasodilators01:23

Antihypertensive Drugs: Vasodilators

Vasodilators, primarily affecting the smooth muscles within arterial and venous walls, are commonly used for hypertension treatment. Medications such as minoxidil and hydralazine primarily target arteries and arterioles, while sodium nitroprusside acts on arterioles and venules. Minoxidil, functioning as a prodrug, is metabolized by hepatic sulfotransferase into its active form, minoxidil sulfate, after oral administration. This metabolite binds to the sulfonylurea receptor (SUR) component of...
Acute Inflammation II: Local and Systemic Effects01:25

Acute Inflammation II: Local and Systemic Effects

Acute inflammation produces a coordinated set of local and systemic changes that limit injury, eliminate pathogens, and initiate repair. These responses arise within minutes of infection, trauma, or chemical insult and are driven by vascular alterations and leukocyte-derived mediators. When the stimulus resolves, the reaction typically abates within days.Local EffectsAt the site of injury, arteriolar vasodilation increases blood flow, resulting in redness and warmth. Simultaneously, increased...
Bacterial Meningitis II: Pathophysiology01:26

Bacterial Meningitis II: Pathophysiology

Bacterial meningitis typically begins when pathogens such as Neisseria meningitidis and Streptococcus pneumoniae colonize the nasopharynx and invade the bloodstream. This process is facilitated by bacterial virulence factors, such as polysaccharide capsules, which resist phagocytosis and complement-mediated killing. Less commonly, bacteria reach the central nervous system via contiguous spread from infections like otitis media or sinusitis, through congenital or acquired dural defects, or...