Related Experiment Video

Updated: Dec 8, 2025

Phenotypic Characterization of Macrophages from Rat Kidney by Flow Cytometry
07:14

Phenotypic Characterization of Macrophages from Rat Kidney by Flow Cytometry

Published on: October 18, 2016

15.2K

Macrophage secretion of miR-106b-5p causes renin-dependent hypertension

J Oh1, S J Matkovich1, A E Riek1

  • 1Department of Medicine, Washington University School of Medicine, St. Louis, MO, USA.

Nature Communications
|September 24, 2020
PubMed

Insights

Impaired vitamin D signaling in myeloid cells drives hypertension by promoting macrophage infiltration and activating renin production. This involves miR-106b-5p secretion, highlighting a new pathway in inflammation-induced hypertension.

Area of Science:

  • Immunology
  • Endocrinology
  • Cardiovascular Research

Background:

  • Myeloid cells are implicated in hypertension.
  • Vitamin D deficiency is linked to inflammation and renin-mediated hypertension.
  • The specific role of myeloid vitamin D signaling in hypertension initiation is unclear.

Purpose of the Study:

  • To investigate if impaired vitamin D signaling in macrophages initiates renin-induced hypertension.
  • To elucidate the mechanisms by which myeloid cells contribute to hypertension.

Main Methods:

  • Conditional knockout mice (KODMAC) lacking myeloid vitamin D receptor were generated.
  • Macrophage infiltration, juxtaglomerular (JG) cell renin production, and miR-106b-5p secretion were analyzed.
  • Bone marrow transplantation studies were performed using KODMAC/miR106b-/- mice.

Main Results:

  • KODMAC mice developed renin-dependent hypertension with vascular macrophage infiltration.
  • Endoplasmic reticulum stress in KODMAC macrophages increased miR-106b-5p secretion.
  • miR-106b-5p stimulated JG cell renin production by repressing E2f1 and Pde3b.
  • miR-106b-5p knockout prevented hypertension in KODMAC macrophage recipients.

Conclusions:

  • Impaired myeloid vitamin D receptor signaling causes hypertension.
  • Macrophage-derived miR-106b-5p is a key mediator in this process.
  • This study identifies a novel mechanism of inflammation-induced hypertension.

More Related Videos

Rapid Depletion of Renal Macrophages Using Human CD59/Intermedilysin Cell Ablation Tool10:15

Rapid Depletion of Renal Macrophages Using Human CD59/Intermedilysin Cell Ablation Tool

Published on: May 9, 2025

545
Isolation and Adoptive Transfer of High Salt Treated Antigen-presenting Dendritic Cells09:29

Isolation and Adoptive Transfer of High Salt Treated Antigen-presenting Dendritic Cells

Published on: March 5, 2019

6.0K

Related Concept Videos

Hypertension II: Pathophysiology01:29

Hypertension II: Pathophysiology

Hypertension is a chronic condition in which the blood's force against artery walls is excessively high, posing risks such as heart disease. The condition's underlying mechanisms involve complex interactions among the cardiovascular, kidney, and autonomic nervous systems.Renin-Angiotensin-Aldosterone System (RAAS): This system significantly influences blood pressure regulation. When blood pressure decreases, the kidneys secrete renin. This enzyme transforms angiotensinogen, a plasma protein,...
529
Hormonal Regulation01:33

Hormonal Regulation

The renin-aldosterone system is an endocrine system which guides the renal absorption of water and electrolytes, thus managing blood pressure and osmoregulation. Activation of the system begins in the kidneys with a small cluster of cells adjacent to the afferent and efferent blood vessels of the renal corpuscle. As the nephrons are filtering blood, juxtaglomerular cells monitor blood pressure. If they detect a decrease in pressure, they release the hormone renin into the bloodstream.
35.2K
Antihypertensive Drugs: Direct Renin Inhibitors01:25

Antihypertensive Drugs: Direct Renin Inhibitors

The renin-angiotensin-aldosterone system (RAAS) is an intricate physiological pathway involving numerous enzymes and hormones, including renin, angiotensin-converting enzyme (ACE), angiotensin I and II, and aldosterone. Imbalances within this system increase the production of angiotensin II and aldosterone. Increased angiotensin II levels promote vasoconstriction and blood pressure elevation. Concurrently, higher aldosterone levels stimulate sodium and water reabsorption in the kidneys,...
1.1K
Hypertension and Regulation of Blood Pressure01:18

Hypertension and Regulation of Blood Pressure

Hypertension, the most common cardiovascular disease, is diagnosed through repeated measurements of elevated blood pressure. Its risks, including damage to the kidney, heart, and brain, are directly proportional to blood pressure levels. Starting from 115/75 mm Hg, the risk of cardiovascular disease doubles with each increment of 20/10 mm Hg. The diagnosis relies on blood pressure measurements, not on patient symptoms, as hypertension is often asymptomatic until end-organ damage is imminent or...
3.5K
Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors01:30

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors

Angiotensin-converting enzyme (ACE), a vital component of the renin-angiotensin-aldosterone system, is abundant in lung endothelial cells. ACE converts the inactive decapeptide, angiotensin I, into the active octapeptide, angiotensin II. This potent vasoconstrictor narrows blood vessels, increasing resistance to blood flow and elevating blood pressure. Angiotensin II also stimulates aldosterone production, encouraging kidney cells to reabsorb more sodium and water from urine, thereby increasing...
2.1K
Antihypertensive Drugs: Angiotensin II Receptor Blockers01:30

Antihypertensive Drugs: Angiotensin II Receptor Blockers

In the renin-angiotensin-aldosterone system, a hormone called angiotensin II plays a crucial role. It binds to the AT1 receptors in vascular smooth muscles coupled with Gq proteins. The activation of these receptors activates an enzyme called phospholipase C, which releases two molecules: inositol trisphosphate and diacylglycerol. These molecules cause a chain reaction that leads to the phosphorylation of myosin light chains and promotes interaction between actin and myosin, leading to smooth...
2.2K