Abstract 214: Protein Restriction Attenuates Intimal Hyperplasia and Alters Blood Lipid Profiles

2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
Christine R Mauro ◽  
Ming Tao ◽  
Peng Yu ◽  
Chengwei Liu ◽  
James Mitchell ◽  
...  
Keyword(s):  
Intimal Hyperplasia ◽  
Surgical Stress ◽  
Blood Lipid ◽  
Outer Diameter ◽  
Internal Elastic Lamina ◽  
Subsequent Removal ◽  
Short Term ◽  
Complete Diet ◽  
Protein Free Diet ◽  
Elastic Lamina

Introduction Dietary restriction (DR: reduced enteral intake without malnutrition) diminishes the acute phase response to surgical stress in preclinical models. We hypothesized that short-term preoperative protein-free DR would attenuate the vascular response to injury (intimal hyperplasia: IH) while perturbing systemic circulating lipids. Methods After 2 weeks of 60% fat kcal diet, 8 week old B6D2F1/J mice had ad lib access to a complete 10% fat kcal diet (n=10) or a reduced calorie, protein-free diet (DR group, n=10) 1 week before induction of IH, then an ad lib complete diet. IH was induced via a validated model placing a nylon suture tie around the distal carotid artery and external 35g needle mandrel (outer diameter=0.14mm). Subsequent removal of the mandrel created a focal area of stenosis (~78% lumen diameter/~85% flow reduction). 4 weeks later, tissues were harvested for morphology and immunohistochemistry for CD45. Separately, serum was collected from mice fed a complete or DR diet for 1 week absent any surgical stress (n=20/group) for mass spectrometry-based lipidomics. Results DR mice showed less intimal area (p = 0.032) vs controls with statistically equivalent intimal leukocyte infiltration. DR mice also had significantly larger internal elastic lamina length (p = 0.003), a remodeling measure. DR serum exhibited significant decreases in certain classes of circulating lipids, including a collapse of multiple triglyceride types. Conclusions One week of protein-free DR dramatically decreased circulating lipids and attenuated arterial IH. Preoperative dietary manipulations may offer a practical means of extending durability of vascular interventions.

scholarly journals Vascular Smooth Muscle Cell Subpopulations and Neointimal Formation in Mouse Models of Elastin Insufficiency

2021 ◽  
Author(s):  
Chien-Jung Lin ◽  
Bridget Hunkins ◽  
Robyn Roth ◽  
Chieh-Yu Lin ◽  
Jessica E. Wagenseil ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Intimal Hyperplasia ◽  
Ascending Aorta ◽  
Specific Cell ◽  
Neointima Formation ◽  
Neointimal Formation ◽  
Internal Elastic Lamina ◽  
Heart Field ◽  
Secondary Heart Field ◽  
Elastic Lamina

Objective: Using a mouse model of Eln (elastin) insufficiency that spontaneously develops neointima in the ascending aorta, we sought to understand the origin and phenotypic heterogeneity of smooth muscle cells (SMCs) contributing to intimal hyperplasia. We were also interested in exploring how vascular cells adapt to the absence of Eln. Approach and Results: We used single-cell sequencing together with lineage-specific cell labeling to identify neointimal cell populations in a noninjury, genetic model of neointimal formation. Inactivating Eln production in vascular SMCs results in rapid intimal hyperplasia around breaks in the ascending aorta’s internal elastic lamina. Using lineage-specific Cre drivers to both lineage mark and inactivate Eln expression in the secondary heart field and neural crest aortic SMCs, we found that cells with a secondary heart field lineage are significant contributors to neointima formation. We also identified a small population of secondary heart field-derived SMCs underneath and adjacent to the internal elastic lamina. Within the neointima of SMC-Eln knockout mice, 2 unique SMC populations were identified that are transcriptionally different from other SMCs. While these cells had a distinct gene signature, they expressed several genes identified in other studies of neointimal lesions, suggesting that some mechanisms underlying neointima formation in Eln insufficiency are shared with adult vessel injury models. Conclusions: These results highlight the unique developmental origin and transcriptional signature of cells contributing to neointima in the ascending aorta. Our findings also show that the absence of Eln, or changes in elastic fiber integrity, influences the SMC biological niche in ways that lead to altered cell phenotypes.

Anchoring Fibrils in Arterial Endothelium

1969 ◽  
Vol 27 ◽  
pp. 274-275
Author(s):  
A. Trillo
Keyword(s):  
Carotid Arteries ◽  
Animal Species ◽  
Cell Layer ◽  
Present Communication ◽  
Internal Elastic Lamina ◽  
Endothelial Cell Layer ◽  
Structural Details ◽  
Rats And Mice ◽  
Arterial Endothelium ◽  
Elastic Lamina

There are conflicting reports regarding some fine structural details of arteries from several animal species. Buck denied the existence of a sub-endothelial space, while Karrer and Keech described a space of variable width which separates the endothelium from the underlying internal elastic lamina in aortas of aging rats and mice respectively.The present communication deals with the ultrastrueture of the interface between the endothelial cell layer and the internal elastic lamina as observed in carotid arteries from rabbits of varying ages.

scholarly journals Elastic Fibers of the Internal Elastic Lamina Are Unraveled But Not Created With Expanding Arterial Diameter in Arteriogenesis

2020 ◽  
Vol 1 ◽  
pp. 247
Author(s):  
Derek Afflu ◽  
Dylan D. McCreary ◽  
Nolan Skirtich ◽  
Kathy Gonzalez ◽  
Edith Tzeng ◽  
...  
Keyword(s):  
Elastic Fibers ◽  
Internal Elastic Lamina ◽  
Arterial Diameter ◽  
Elastic Lamina

The Psychiatric Aspects of Temporal Arteritis

1952 ◽  
Vol 98 (411) ◽  
pp. 280-286 ◽  
Author(s):  
R. Vereker
Keyword(s):  
Virus Infection ◽  
Giant Cell Arteritis ◽  
Temporal Arteritis ◽  
Giant Cells ◽  
Low Grade ◽  
Internal Elastic Lamina ◽  
Temporal Arteries ◽  
The Media ◽  
Cranial Arteries ◽  
Elastic Lamina

Temporal arteritis, also called giant cell arteritis, or cranial arteritis, was first described in 1932 by Horton and Magath. This syndrome is caused by a reversible inflammation of the cranial arteries, especially the temporal arteries (which are visibly inflamed), causing headache, mental and neurological disturbances as well as general toxic signs, and almost always occurring after the age of fifty-five years.Pathology.—In the arteries involved there is a subacute inflammation of the adventitia and media with focal necrosis of the media, fragmentation and destruction of the internal elastic lamina with gross hypertrophy of the intima, often leading to occlusion of the vessel. In many cases giant cells are found in the media. Besides the cranial arteries other vessels are sometimes involved, e.g., the carotids (Scott and Maxwell 1941; Gilmour 1941), subclavian, coronary and femoral arteries (Cookeet al., 1946), post-auricular (Dick and Freeman 1940).Aetiologyis unknown. There is no evidence of tuberculosis or syphilis. A low-grade bacterial or virus infection of the arteries has been postulated, but repeated bacteriological examinations of the biopsied arteries have failed to isolate any organisms. The predilection which the condition shows for the temporal and cranial arteries is unexplained.

Abstract W P73: Inside Intramural Thrombus Formation with Inflammatory Reactions Is Relevant to the Rupture of Cerebral Aneurysms

Stroke ◽  
2015 ◽  
Vol 46 (suppl_1) ◽  
Author(s):  
Yusuke Shimoda ◽  
Naoki Nakayama ◽  
Masaaki Hokari ◽  
Takeo Abumiya ◽  
Hideo Shichinohe ◽  
...  
Keyword(s):  
Thrombus Formation ◽  
Cerebral Aneurysms ◽  
Histopathological Finding ◽  
Internal Elastic Lamina ◽  
Electron Microscopic ◽  
Inflammatory Reactions ◽  
Aneurysmal Wall ◽  
The Common ◽  
Collagen Layer ◽  
Elastic Lamina

Background and Purpose: Although recent researches on cerebral aneurysms (CAs) have been performed with the hydrodynamic or the molecular biological technique, the mechanisms of rupture are not fully understood. The aim of this study is to assess the mechanism by a comparison between ruptured and un-ruptured CAs with histopathological and electron-microscopic analysis. Methods: We analyzed 33 CAs (24 ruptured, 9 un-ruptured) collected surgically after neck clipping. As for the ruptured CAs, we operated them within 24 hours from the onset. HE staining, Elastica Masson staining, PTAH staining, and CD68 immunohistochemical staining were performed with paraffin sections. Morphological analysis with Scanning Electron Microscopy (SEM) was performed with 6 CAs (3 ruptured, 3 un-ruptured). Results: The common histopathological finding in both ruptured and un-ruptured CAs was that the aneurysmal wall consisted mostly of thick collagen layer without normal internal elastic lamina and media. The characteristic histopathological finding in ruptured CAs was inside intramural thrombus formation with infiltration of CD68 positive cells at the rupture point. The common SEM finding in both ruptured and un-ruptured CAs was the denudation of endothelial cells and the exposure of a subendothelial amorphous or a fibrous surface. The characteristic SEM finding in ruptured CAs was the cluster formation of thick fibrin fibers with incorporation of macrophages and platelets. Conclusions: While the endothelial denudation, the disappearance of internal elastic lamina and media, and the predominance of collagen layer in the aneurysmal wall were common in both ruptured and un-ruptured CAs, inside intramural thrombus formation with inflammatory reactions was characteristic only in ruptured CAs. This result suggests that thrombo-inflammatory reactions in CAs may act as a trigger for ruptures.

Functional medial thickening and folding of the internal elastic lamina in coronary spasm

2011 ◽  
Vol 300 (2) ◽  
pp. H423-H430 ◽  
Author(s):  
Yasumi Uchida ◽  
Yasuto Uchida ◽  
Akimasa Matsuyama ◽  
Atsushi Koga ◽  
Yuko Maezawa ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Structural Changes ◽  
Light And Electron Microscopy ◽  
Coronary Spasm ◽  
Cellular Level ◽  
Internal Elastic Lamina ◽  
Circular Smooth Muscle ◽  
The Media ◽  
Medial Thickening ◽  
Elastic Lamina

Although there are a number of studies on vasospastic angina, the structural changes at the cellular level that occur in the coronary arterial wall during spasm are not well known. Coronary spasm was induced by brushing the coronary adventitia in nine anesthetized beagles, and structural changes in the spastic coronary segments were examined by light and electron microscopy, making comparisons with the adjacent nonspastic segments. The % diameter stenosis of the spastic segments as measured angiographically was 79.4 ± 12% (mean ± SD). Light microscopic changes in the spastic and nonspastic segments were as follows: medial thickness 1,512 vs. 392 μm ( P < 0.0001) and % diameter and % area stenoses of spastic segment 81.0% and 96.5%, respectively, indicating that spasm was induced by medial thickening. Circular smooth muscle cells (SMCs) in the media were arranged in parallel with the internal (IEL) and external (EEL) elastic lamina in nonspastic segments but radially rearranged in spastic segments. SMCs were classified by their patterns of connection to IEL into six types by electron microscopy. Of these, three contracted and pulled the IEL toward the EEL, causing folding of the IEL and waving of EEL resulting in thickening of the media and narrowing of the lumen. We conclude that coronary spasm was elicited by radial rearrangement of the medial SMCs due to their own contraction and resultant medial thickening and folding of IEL, creating a piston effect to narrow the lumen, i.e., spasm.

Abstract 270: Acute Reductions in Wall Strain Precede Formation of Intimal Hyperplasia

2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
John T Favreau ◽  
Chengwei Liu ◽  
Peng Yu ◽  
Christine Mauro ◽  
Ming Tao ◽  
...  
Keyword(s):  
Carotid Artery ◽  
Murine Model ◽  
Intimal Hyperplasia ◽  
Arterial Wall ◽  
Lumen Area ◽  
Subsequent Removal ◽  
Distal Mouse ◽  
Intimal Thickness ◽  
Acute Changes ◽  
Focal Stenosis

Intimal hyperplasia (IH) remains the major culprit in revascularization failures. We aimed to unravel relationships between acute changes in circumferential arterial wall strain and genesis of IH. Methods To induce IH, we employed a validated model using a 9-0 nylon suture tie around the distal mouse common carotid artery (n=10) and an external 35-gauge needle mandrel (OD=0.14mm), with subsequent removal of the mandrel to create a distal common carotid focal stenosis (~78% lumen diameter/~85% flow reduction). Wall strains were measured in three, 1 mm wide regions along the vessel proximal to the focal stenosis at pre-op day 1 and at post-op day 4 (before detectable IH) using Vevo 2100 ultrasonography with VevoVasc software. At post-op day 28, arteries were perfusion fixed and IH was assessed in the same regions as those where strain was analyzed. Strain and morphology were also assessed in the contralateral control artery. Results Decreased wall strain was noted in all regions proximal to the focal stenosis from 0.26 ± 0.01 to 0.11 ± 0.02 (p<0.001) with no change in the control artery from pre-op to post-op day 4 (p=0.45). Based on a strain level histogram, vessels were divided into groups with strain ≤0.1 and >0.1. All segments (n = 13) with wall strain ≤0.1 at post-op day 4 had significant IH at day 28. In regions with strains >0.1 at day 4, only 30% had IH at day 28. The average pre-op strains were identical in >0.1 and ≤0.1 strain groups (0.27 ± 0.09 and 0.27 ± 0.08). Mean intimal thickness in vessels with strain ≤0.1 was 32 ± 20 μm, significantly greater than 8.0 ± 16 μm in the group with strain >0.1 (p<0.01). To further understand the mechanisms underlying changes in strain, systolic and diastolic lumen areas were assessed. Although systolic lumen areas in both >0.1 and ≤0.1 groups remained unchanged from pre-op to post-op day 4 (p=0.46), diastolic area was significantly increased in regions with post-op day 4 strain ≤0.1 (p=0.04) but remained unchanged in mice with post-op day 4 strain >0.1 (p=0.67). Conclusions Acute reduction in wall strain precedes the formation of IH in this murine model and this change is primarily caused by an increase in diastolic lumen area. Manipulations of wall strain offer a strategy to prevent and attenuate occlusive IH lesions after revascularizations.

Sign in / Sign up

Export Citation Format

Share Document