C57BL/6, ApoE−/−or ApoE−/−(WD) mice were anesthetized and their vasculature was perfused by cardiac puncture with PBS containing 20 U/ml of heparin to remove blood from all vessels. Under a dissection microscope, we carefully harvested whole aortas by pulling off all of the adipose tissue and collecting all aortic layers including the adventitia. To fully characterize the collected aortas, we measured aortic wall thickness and adventitial thickness in paraffin-cut sections. In addition, the dissected aortas were weighed to control the total amount of collected aortic tissues. Harvested aortas were microdissected and digested with 125 U/ml collagenase type XI, 60 U/ml hyaluronidase type I-s, 60 U/ml DNase1, and 450 U/ml collagenase type I (all enzymes were obtained from Sigma-Aldrich) in PBS containing 20 mM Hepes at 37°C for 1 h. A cell suspension was obtained by mashing the aorta through a 70-μm strainer. Cells were incubated with Abs for 20 min at 4°C, washed twice, and incubated with secondary Abs for an additional 20 min. After washing, immunofluorescence was detected by flow cytometry (FACSCalibur or CyanADP), data were analyzed using WinMDI (The Scripps Research Institute) or FlowJO (Tree Star Inc.) software. Abs used were as follows: allophycocyanin (APC)-Cy7 or PE-Texas red-CD45, FITC, PE or PerCP-CD3, FITC, APC-TCRβ, PE-Cy5 or APC-CD19, PE-B220, PE-I-Ab, PerCP-Cy5.5-Mac-1, PE or APC-CD11c (all Abs were obtained from BD Biosciences) and FITC-CD68 (Serotec). In some experiments, the aortas from two to three mice were pooled and analyzed. In some experiments, LN or spleens from C57BL/6 mice were collected and split in two parts: one part of pLN (or spleen) was treated with the enzyme cocktail (see previous paragraph) and the other was kept at 4°C. After 1 h, the expression of CD45, TCR, CD19, I-Ab antigens was determined by flow cytometry.
Adventitia
Adventitia is the outermost layer of blood vessels, consisting of connective tissue that provides structural support and helps regulate blood flow.
It plays a crucial role in maintaining vascular homeostasis and responding to various physiological and pathological stimuli.
The adventitia is an important target for research on vascular biology and disease, as it can influence the development and progression of cardiovascular conditions.
Researchers can utilize PubCompare.ai's AI-powered tools to optimize their Adventitia research protocols, locate the best available protocols, and uncover hidden insights to advance their understanding of this critical vascular structure.
It plays a crucial role in maintaining vascular homeostasis and responding to various physiological and pathological stimuli.
The adventitia is an important target for research on vascular biology and disease, as it can influence the development and progression of cardiovascular conditions.
Researchers can utilize PubCompare.ai's AI-powered tools to optimize their Adventitia research protocols, locate the best available protocols, and uncover hidden insights to advance their understanding of this critical vascular structure.
Most cited protocols related to «Adventitia»
Adventitia
allophycocyanin
Antigen T Cell Receptor, beta Chain
Aorta
ApoE protein, human
Blood Vessel
Cells
Collagenase
Collagenase, Clostridium histolyticum
CY5.5 cyanine dye
Dissection
Enzymes
Flow Cytometry
Fluorescein-5-isothiocyanate
Heart
Heparin
HEPES
Hyaluronidase
I-antigen
Immunofluorescence
Macrophage-1 Antigen
Mice, Inbred C57BL
Microscopy
Mus
Paraffin
Punctures
Spleen
Tissue, Adipose
Trees
Under sterile conditions, anaesthetized SD rats were placed in the supine position and their chests were opened. The thoracic aorta was removed and transferred to a culture dish with cold (4°C) DMEM (Figure 1A ). After removal of the fat tissue around the artery (Figure 1B ), the artery was longitudinally cut and placed in another cell culture dish containing DMEM (Figure 1C ). Then, we used a pair of ophthalmic curved tweezers to scrape the intima softly to get rid of endothelial cells (Figure 1D ). Later, we did not separate the adventitia or directly cut the artery into small tissue blocks. Two pairs of ophthalmic curved tweezers were used: one to press the artery to fix it and another to separate the media from the artery by pressing and pushing the artery with its blunt back side (Figure 2 ). After half of the media was removed, the same method was used to get the other half. Then, the media was cut into approximately 1-mm squares and transferred into cell culture plates. The plates were placed in a cell culture chamber for about 4 h to let the small tissue blocks adhere to the plates. DMEM containing 20% FBS was carefully added and the tissue blocks were incubated in the cell culture chamber without disturbance for the first 5 days.
In the traditional tissue explants method, all the steps were similar, and after the fat tissue was removed, the artery was directly cut into small tissue blocks and transferred to cell culture plates without removal of the adventitia.
In the enzyme digestion method, after the fat tissue was removed, the aorta was digested with 1 mg/mL collagenase II and 100 μg/mL elastase at 37°C for 1 h. Later, the cells were pelleted and plated in DMEM with 20% FBS. The next morning, the cells were washed with PBS 3 times and the media were refreshed every 48 h.
The A7r5 cell line has been widely used in vitro to study the physiology and pathophysiology of VSMCs [13 (link),14 (link)]. However, it has lost some VSMCs selectivity and has many differences from primary cultured VSMCs. Therefore, we chose the A7r5 cell line to compare its viability with primary cultured VSMCs.
The VSMCs obtained by the above methods (the new tissue explants method, the traditional tissue explants method, the enzyme digestion method, and A7r5 cell line) were identified through morphology and immunofluorescence detection of SM-actin. The purity of the VSMCs was tested through multiple fluorescent staining with DAPI and SM-actin antibody.
In the traditional tissue explants method, all the steps were similar, and after the fat tissue was removed, the artery was directly cut into small tissue blocks and transferred to cell culture plates without removal of the adventitia.
In the enzyme digestion method, after the fat tissue was removed, the aorta was digested with 1 mg/mL collagenase II and 100 μg/mL elastase at 37°C for 1 h. Later, the cells were pelleted and plated in DMEM with 20% FBS. The next morning, the cells were washed with PBS 3 times and the media were refreshed every 48 h.
The A7r5 cell line has been widely used in vitro to study the physiology and pathophysiology of VSMCs [13 (link),14 (link)]. However, it has lost some VSMCs selectivity and has many differences from primary cultured VSMCs. Therefore, we chose the A7r5 cell line to compare its viability with primary cultured VSMCs.
The VSMCs obtained by the above methods (the new tissue explants method, the traditional tissue explants method, the enzyme digestion method, and A7r5 cell line) were identified through morphology and immunofluorescence detection of SM-actin. The purity of the VSMCs was tested through multiple fluorescent staining with DAPI and SM-actin antibody.
Actins
Adventitia
Aorta
Arterial Media
Arterial Occlusion
Arteries
Cell Culture Techniques
Cell Lines
Cells
Chest
Collagenase
Common Cold
Cultural Evolution
DAPI
Digestion
Endothelial Cells
Enzymes
Fluorescent Antibody Technique
Genetic Selection
Hyperostosis, Diffuse Idiopathic Skeletal
Immunoglobulins
Pancreatic Elastase
physiology
Rattus norvegicus
Sterility, Reproductive
Thoracic Aorta
Tissue, Adipose
Tissues
Tunica Intima
Type II Mucolipidosis
Adventitia
Aneurysm
Aorta
Caucasoid Races
Males
Normal Saline
Phosphates
Radius
Subclavian Artery
Thoracic Aorta
Tunica Intima
Adventitia
Arteries
Carotid Arteries
Common Carotid Artery
Diastole
DNA Replication
Internal Carotid Arteries
Medulla Oblongata
Plaque, Atherosclerotic
Sinus, Carotid
Stenosis
Tablet
Transducers
Tunica Intima
Ultrasonography
Ultrasonography, Carotid Arteries
Vision
Adventitia
Allelic Imbalance
Aorta
Biopsy
Carotid Arteries
Dental Plaque
Exons
External Lateral Ligament
Females
Fibroblasts
Gastrojejunostomy
Gene Expression
Gene Expression Regulation
Genotype
Healthy Volunteers
Homo sapiens
Liver
Macrophage
Mammary Arteries
Monocytes
Omentum
Operative Surgical Procedures
Patients
Single Nucleotide Polymorphism
Skin
Subcutaneous Fat
Susceptibility, Disease
Tissues
Twins
Most recents protocols related to «Adventitia»
The measurements of carotid atherosclerosis had been described previously [24 (link)]. In brief, we used high-resolution B-mode ultrasonography systems (GE Healthcare Vivid 7 and Vivid E9; General Electric Company, Milwaukee, USA) and followed the protocol recommended by the American Society of Echocardiography [25 (link)] to obtain the transverse and cross-sectional ultrasound images of the left and right carotid arteries. The thickness between the lumen-intima and media-adventitia interfaces was measured blindly by using automatic contouring software (GE Healthcare EchoPAC version 112.0.2; General Electric-Vingmed, Horten, Norway). In the study, a plaque was defined as a focal protrusion 50% greater than the surrounding vessel wall, an intima-media thickness (IMT) ≥ 1.5 mm, or local thickening ≥ 0.5 mm [26 ].
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Adventitia
Blood Vessel
Carotid Arteries
Carotid Atherosclerosis
Dental Plaque
Echocardiography
Electricity
Tunica Intima
Ultrasonography
The ablated veins harvested after autopsy were irrigated with normal saline. They were immersed and shaded in a 2% 2,3,5-triphenyltetrazolium chloride (TTC) (Sigma) solution and incubated for 1 hour at 40 ℃. After the staining was completed, the veins were sectioned longitudinally and completely unfolded. The exposed ablated site was macroscopically checked, and photographs were taken.
TTC-stained femoral/cephalic veins were fixed in 10% neutral-buffered formalin. Each fixed tissue was rinsed in tap water for 24 hours to completely remove the fixative from the tissue. For tissue dehydration, the tissue was gradually dehydrated using high-concentration ethanol of 70%–100%, and then a paraffin block was produced by clearing with xylene. The prepared block was cut to a thickness of 5 µm using a microtome to prepare slides. The slides were stained with H&E for microscopic evaluation.
Verifying the nonstained area in the vein subjected to TTC staining identified the surviving and damaged areas in the venous endothelium, making it easier to select the area to be examined under the microscope. The part that was not stained with TTC was assessed as the part where vein injury occurred through ablation.
The vessel injury score analyzed based on H&E staining was also used to objectively evaluate the ablating effect. Vessel injury scores were measured at 3 sites per harvested ablated vein. After scanning the entire tissue made of slides with a scanner, the damaged area was visually checked. This method was applied by modifying that of a previous study [3 (link)]. The criteria were assigned according to injury severity from 1 (least injury) to 4 (most injury): 1, endothelial cell coverage; 2, medial smooth muscle cell loss; 3, internal and external elastic lamina disruption; and 4, adventitia disruption. Scoring was comprehensively performed by a pathologist through evaluating the damaged area that each criterion had inflicted on the tissue.
TTC-stained femoral/cephalic veins were fixed in 10% neutral-buffered formalin. Each fixed tissue was rinsed in tap water for 24 hours to completely remove the fixative from the tissue. For tissue dehydration, the tissue was gradually dehydrated using high-concentration ethanol of 70%–100%, and then a paraffin block was produced by clearing with xylene. The prepared block was cut to a thickness of 5 µm using a microtome to prepare slides. The slides were stained with H&E for microscopic evaluation.
Verifying the nonstained area in the vein subjected to TTC staining identified the surviving and damaged areas in the venous endothelium, making it easier to select the area to be examined under the microscope. The part that was not stained with TTC was assessed as the part where vein injury occurred through ablation.
The vessel injury score analyzed based on H&E staining was also used to objectively evaluate the ablating effect. Vessel injury scores were measured at 3 sites per harvested ablated vein. After scanning the entire tissue made of slides with a scanner, the damaged area was visually checked. This method was applied by modifying that of a previous study [3 (link)]. The criteria were assigned according to injury severity from 1 (least injury) to 4 (most injury): 1, endothelial cell coverage; 2, medial smooth muscle cell loss; 3, internal and external elastic lamina disruption; and 4, adventitia disruption. Scoring was comprehensively performed by a pathologist through evaluating the damaged area that each criterion had inflicted on the tissue.
Adventitia
Autopsy
Endothelial Cells
Endothelium
Ethanol
Fixatives
Formalin
Injuries
Microscopy
Microtomy
Myocytes, Smooth Muscle
Normal Saline
Paraffin
Pathologists
Tissues
triphenyltetrazolium chloride
Vascular System Injuries
Vein, Femoral
Veins
Xylene
Histological studies were performed on carotid arteries fixed with 10% buffered formalin under pressure (100 mmHg) in vivo for 2 h. Fixed specimens were embedded in paraffin following regular procedures. Five micrometre sections were stained with Sirius Red and Picrosirius Red (PSR) for collagen. PSR sections were imaged under cross-polarized light (darkfield) to observe collagen birefringence. Images were acquired on an Olympus BX/51 microscope using an Olympus DP70 digital camera (cellSens Dimension) under a × 40 magnification objective. The area fraction of collagen was based on total fibrillar collagen. A custom MATLAB script was used to extract layer-specific (media or adventitia) wall percentages as well as the proportions of thick (red) and thin (orange–yellow–green) birefringent collagen fibres.16 (link),17 (link)For integrin αv subunit immunostaining, rabbit polyclonal antibodies against integrin αv subunit, biotinylated goat anti-rabbit immunoglobulins, HRP-conjugated streptavidin, and 3,3′-diaminobenzidine (DAB) substrate (see Supplementary material online , Tables S7 and S8 ) were used. Composition of the arterial wall and the media cross-sectional area (MCSA) were determined using a Nikon NIS-Elements Basic Research microscope imaging software as described previously.18 (link)Immunofluorescence staining on 8 µm cryo-sections fixed with 4% paraformaldehyde or cooled acetone for 5 min was performed with specific antibodies as described previously.14 (link) Briefly, sections were incubated with primary antibodies at 4°C overnight after permeabilization with 0.2% Triton X100 for 10 min and blocking with 5% bovine serum albumin (BSA) for 1 h. After washing in PBS-Tween 20, sections were incubated with fluorescent-conjugated secondary antibodies. A complete list of antibodies is provided in Supplementary material online , Table S8 . Image acquisition was on a Leica TCS SP5 confocal microscope (Leica, Wetzlar, Germany) with the same depth of field and with identical settings for laser, gain, and offset intensity.
Acetone
Adventitia
Antibodies
Antibodies, Anti-Idiotypic
Arteries
Birefringence
Carotid Arteries
Collagen
Fibrillar Collagen
Fibrosis
Fingers
Fluorescent Antibody Technique
Formalin
Goat
Integrin alphaV
Light
Microscopy
Microscopy, Confocal
Paraffin Embedding
paraform
Pressure
Protein Subunits
Rabbits
Serum Albumin, Bovine
Streptavidin
Triton X-100
Tween 20
Smooth muscle cells were cultured from the medial layer of human aortic samples by enzymatic digestion. To prepare an isolated sample of the media, the endothelial layer of the aorta was removed by scraping the luminal surface gently with a scalpel. The tissue was washed in PBS, and then the adventitia and outer-most medial layers were peeled away with forceps. The remaining medial fragment was washed with PBS, and then used for the enzymatic digestion.
The enzymatic solution was a combination of 830 μl of M199 Media (ThermoFisher Scientific, 11150059; +0.5% FBS + 1% penicillin/streptomycin), 150 μl of Liberase™ (Roche, 05401020001) and 30 μl of DNAse. The prepared aortic media sample was cut into ∼1 × 1 cm fragments and added to a 1.5 ml Eppendorf tube containing the enzymatic solution. The sample was then placed in a SMC incubator (37°C, 5% CO2, 95% humidity) for 2 h. After the incubation, the digested supernatant was collected through a cell strainer and kept on ice until after the final incubation period. The undigested tissue was placed in a new Eppendorf tube with fresh enzymatic solution. The process was repeated for a second digestion, with an incubation period of 1.5 h. The supernatant from the second digestion was combined with that of the first, and the solution was then centrifuged at 750 RPM for 6 min at 4°C. The ensuing cell pellet was reconstituted in M199 media (+10% FBS + 1% penicillin/streptomycin), and the cells were plated on 0.4% gelatin-coated 60 mm cell culture dishes (Gelatin Type B Powder, Sigma-Aldrich, G9391; ThermoFisher Scientific Cell Culture Petri Dishes, 150340). The SMCs were maintained in the SMC incubator, as above.
The SMC media was changed 24 h after the isolation was completed, and then every 2 days until the cells reached confluence. When confluence was reached, the cells were trypsinized (Trypsin/EDTA solution, ThermoFisher Scientific, R001100) and plated on coverslips for immunocytochemistry (cell passage 1), or were plated on a fresh culture dish for continued growth and subsequent analysis of cellular senescence. For immunocytochemistry, serum was withdrawn from culture when the cells reached 80% confluence, and the cells were fixed with 4% paraformaldehyde after 72 h. For cellular senescence studies, the cells were re-platted each time confluence was reached until the cells stopped growing.
The enzymatic solution was a combination of 830 μl of M199 Media (ThermoFisher Scientific, 11150059; +0.5% FBS + 1% penicillin/streptomycin), 150 μl of Liberase™ (Roche, 05401020001) and 30 μl of DNAse. The prepared aortic media sample was cut into ∼1 × 1 cm fragments and added to a 1.5 ml Eppendorf tube containing the enzymatic solution. The sample was then placed in a SMC incubator (37°C, 5% CO2, 95% humidity) for 2 h. After the incubation, the digested supernatant was collected through a cell strainer and kept on ice until after the final incubation period. The undigested tissue was placed in a new Eppendorf tube with fresh enzymatic solution. The process was repeated for a second digestion, with an incubation period of 1.5 h. The supernatant from the second digestion was combined with that of the first, and the solution was then centrifuged at 750 RPM for 6 min at 4°C. The ensuing cell pellet was reconstituted in M199 media (+10% FBS + 1% penicillin/streptomycin), and the cells were plated on 0.4% gelatin-coated 60 mm cell culture dishes (Gelatin Type B Powder, Sigma-Aldrich, G9391; ThermoFisher Scientific Cell Culture Petri Dishes, 150340). The SMCs were maintained in the SMC incubator, as above.
The SMC media was changed 24 h after the isolation was completed, and then every 2 days until the cells reached confluence. When confluence was reached, the cells were trypsinized (Trypsin/EDTA solution, ThermoFisher Scientific, R001100) and plated on coverslips for immunocytochemistry (cell passage 1), or were plated on a fresh culture dish for continued growth and subsequent analysis of cellular senescence. For immunocytochemistry, serum was withdrawn from culture when the cells reached 80% confluence, and the cells were fixed with 4% paraformaldehyde after 72 h. For cellular senescence studies, the cells were re-platted each time confluence was reached until the cells stopped growing.
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Adventitia
Aorta
Cell Culture Techniques
Cells
Cellular Senescence
Deoxyribonucleases
Digestion
Edetic Acid
Endothelium
Enzymes
Forceps
Gelatins
Homo sapiens
Humidity
Hyperostosis, Diffuse Idiopathic Skeletal
Immunocytochemistry
isolation
Liberase
Myocytes, Smooth Muscle
paraform
Penicillins
Pepsin A
Phenobarbital
Powder
Serum
Streptomycin
Tissues
Trypsin
Mouse aortic SMCs were isolated as the following steps: Briefly, mouse aortas were separated and the peri‐aortic adipose tissue was cleaned as much as could be to avoid possible contamination. The adventitia was digested with 2 mg mL−1 collagenase type‐II (LS004177; Worthington Biochemical Corp.) at 37 °C in water bath for 10 min. Aortas were then cut into small pieces and digested in 1 mg mL−1 collagenase type‐II at 37 °C for 45 min with shaking every 15 min. After digestion, 10 mL of DMEM were added containing 10% fetal bovine serum (FBS) to stop. After centrifugation, cells were resuspended with fresh media (DMEM with 10% FBS and 1% penicillin and streptomycin) and plated on a 60 mm culture dish. Media was changed every 2 d. When the SMCs became confluent, the cells were transferred to new cell culture plates. Cells will be ready to use after passage 4. SMCs were pretreated with or without EOS lysates from WT mice at 1 × 106 EOS mL−1, ILC2 lysates from WT Il13−/−and Il5−/− mice at 2 × 104 ILC2 mL−1, and different concentrations of mouse recombinant IL5 (10, 100, and 200 ng mL−1, 405‐ML, R&D Systems, Minneapolis, MN) and mouse recombinant IL13 (10 ng mL−1, 575904, BioLegend) for 24 h. SMCs were then incubated with 10 ng mL−1 TGF‐β, 20% FBS, and PDTC respectively. Immunoblot analysis tested the expression of p‐Smad2 (1:1000, 3108S, Cell Signaling Technology), p‐Smad3 (1:1000, ab52903, Abcam), Smad2 (1:1000, 5339S, Cell Signaling Technology), Smad3 (1:500, 9523S, Cell Signaling Technology), p‐AKT (1:1000, 9271S, Cell Signaling Technology), cleaved caspase‐3 (1:500, 9661L, Cell Signaling Technology), and GAPDH (1:3000, 2118S, Cell Signaling Technology). Immunoblots were quantified by gel density analysis using the Image J software.
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Adventitia
Aorta
Bath
Caspase 3
Cell Culture Techniques
Cells
Centrifugation
collagenase 1
Digestion
Fetal Bovine Serum
GAPDH protein, human
Hyperostosis, Diffuse Idiopathic Skeletal
Immunoblotting
Interleukin-13
Mus
Neutrophil Collagenase
Penicillins
prolinedithiocarbamate
SMAD2 protein, human
SMAD3 protein, human
Streptomycin
TGF-beta1
Tissue, Adipose
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More about "Adventitia"
Adventitia, the outermost layer of blood vessels, is a crucial component of the vascular system.
This connective tissue provides structural support and helps regulate blood flow, playing a vital role in maintaining vascular homeostasis and responding to various physiological and pathological stimuli.
Understanding the adventitia is paramount for researchers studying vascular biology and disease, as it can influence the development and progression of cardiovascular conditions.
To optimize Adventitia research protocols, researchers can utilize PubCompare.ai's AI-powered tools.
These advanced comparison tools enable scientists to locate the best available protocols from literature, pre-prints, and patents, streamlining their research process.
By incorporating data-driven recommendations and uncovering hidden insights, researchers can elevate their understanding of this critical vascular structure.
The adventitia is composed of various cell types, including fibroblasts, vascular smooth muscle cells, and inflammatory cells.
These cells interact with the extracellular matrix, which is rich in collagen and elastin fibers.
Researchers often use techniques like Collagenase type II and Elastase to study the adventitial composition and its role in vascular function.
Imaging modalities, such as the IU22 ultrasound system and the Vevo 2100, have been instrumental in visualizing and analyzing the adventitia.
These tools provide valuable insights into the structure and dynamics of this vascular layer, allowing researchers to better understand its involvement in cardiovascular pathologies.
In addition to these specialized techniques, researchers may also utilize common cell culture media like DMEM and supplements like Penicillin/streptomycin to maintain and study adventitial cells in vitro.
Staining methods, such as Oil Red O, can be employed to investigate lipid accumulation and other cellular features within the adventitia.
By leveraging PubCompare.ai's AI-powered tools and incorporating a wide range of techniques and resources, researchers can optimize their Adventitia research protocols, uncover hidden insights, and advance their understanding of this crucial vascular structure.
The insights gained from this research can contribute to the development of novel therapies and improved patient outcomes in the field of cardiovascular medicine.
This connective tissue provides structural support and helps regulate blood flow, playing a vital role in maintaining vascular homeostasis and responding to various physiological and pathological stimuli.
Understanding the adventitia is paramount for researchers studying vascular biology and disease, as it can influence the development and progression of cardiovascular conditions.
To optimize Adventitia research protocols, researchers can utilize PubCompare.ai's AI-powered tools.
These advanced comparison tools enable scientists to locate the best available protocols from literature, pre-prints, and patents, streamlining their research process.
By incorporating data-driven recommendations and uncovering hidden insights, researchers can elevate their understanding of this critical vascular structure.
The adventitia is composed of various cell types, including fibroblasts, vascular smooth muscle cells, and inflammatory cells.
These cells interact with the extracellular matrix, which is rich in collagen and elastin fibers.
Researchers often use techniques like Collagenase type II and Elastase to study the adventitial composition and its role in vascular function.
Imaging modalities, such as the IU22 ultrasound system and the Vevo 2100, have been instrumental in visualizing and analyzing the adventitia.
These tools provide valuable insights into the structure and dynamics of this vascular layer, allowing researchers to better understand its involvement in cardiovascular pathologies.
In addition to these specialized techniques, researchers may also utilize common cell culture media like DMEM and supplements like Penicillin/streptomycin to maintain and study adventitial cells in vitro.
Staining methods, such as Oil Red O, can be employed to investigate lipid accumulation and other cellular features within the adventitia.
By leveraging PubCompare.ai's AI-powered tools and incorporating a wide range of techniques and resources, researchers can optimize their Adventitia research protocols, uncover hidden insights, and advance their understanding of this crucial vascular structure.
The insights gained from this research can contribute to the development of novel therapies and improved patient outcomes in the field of cardiovascular medicine.