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passage 3 4 huvec  (PromoCell)


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    Structured Review

    PromoCell passage 3 4 huvec
    IGF-1 receptor over-expression reduces paracellular leakage and LDL-cholesterol uptake in human endothelial cells via its kinase domain. ( A ) Schema of lentiviral constructs used to achieve doxycycline-inducible WT or kinase-dead (K1003R) IGF-1R over-expression. ( B ) WT and K1003R IGF-1R protein expression are increased approximately three-fold by doxycycline. ( C ) Representative images of <t>HUVEC</t> VE-Cadherin with either WT or K1003R IGF-1R over-expression (VE-Cadherin—red, DAPI—blue). D ) VE-Cadherin junction thickness is reduced in confluent HUVEC exposed to 100 μM hydrogen peroxide over-expressing WT IGF-1R, but remains unchanged with cells over-expressing K1003R IGF-1R. ( E ) VE-Cadherin junction area is similar in confluent HUVEC over-expressing WT or K1003R IGF-1R. ( F ) Paracellular leakage of 40 kDa FITC-Dextran is reduced in HUVEC over-expressing WT IGF-1R, but not K1003R, IGF-1R. G ) Uptake of BODIPY-labelled LDL-cholesterol is reduced in HUVEC over-expressing WT IGF-1R, but not K1003R, IGF-1R (representative images on left; BODIPY—green, DAPI—blue). ( H ) Representative immunoblots of YAP/TAZ and loading controls in nuclear and cytosolic lysates, accompanied by quantification of normalized nuclear TAZ expression and nuclear:cytosolic TAZ ratio, showing reduced nuclear TAZ in HUVEC over-expressing WT vs. K1003R IGF-1R. ns denotes non-specific band in α-tubulin blot. Data expressed as mean (SEM). * P < 0.05; n = 3, 3 in a–g and n = 4, 4 in h. All statistical comparisons are made with unpaired Student’s t -tests.
    Passage 3 4 Huvec, supplied by PromoCell, used in various techniques. Bioz Stars score: 96/100, based on 213 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/passage+3+4+huvec/pmc12236071-155-0-3?v=PromoCell
    Average 96 stars, based on 213 article reviews
    passage 3 4 huvec - by Bioz Stars, 2026-06
    96/100 stars

    Images

    1) Product Images from "Endothelial insulin-like growth factor-1 signalling regulates vascular barrier function and atherogenesis"

    Article Title: Endothelial insulin-like growth factor-1 signalling regulates vascular barrier function and atherogenesis

    Journal: Cardiovascular Research

    doi: 10.1093/cvr/cvaf055

    IGF-1 receptor over-expression reduces paracellular leakage and LDL-cholesterol uptake in human endothelial cells via its kinase domain. ( A ) Schema of lentiviral constructs used to achieve doxycycline-inducible WT or kinase-dead (K1003R) IGF-1R over-expression. ( B ) WT and K1003R IGF-1R protein expression are increased approximately three-fold by doxycycline. ( C ) Representative images of HUVEC VE-Cadherin with either WT or K1003R IGF-1R over-expression (VE-Cadherin—red, DAPI—blue). D ) VE-Cadherin junction thickness is reduced in confluent HUVEC exposed to 100 μM hydrogen peroxide over-expressing WT IGF-1R, but remains unchanged with cells over-expressing K1003R IGF-1R. ( E ) VE-Cadherin junction area is similar in confluent HUVEC over-expressing WT or K1003R IGF-1R. ( F ) Paracellular leakage of 40 kDa FITC-Dextran is reduced in HUVEC over-expressing WT IGF-1R, but not K1003R, IGF-1R. G ) Uptake of BODIPY-labelled LDL-cholesterol is reduced in HUVEC over-expressing WT IGF-1R, but not K1003R, IGF-1R (representative images on left; BODIPY—green, DAPI—blue). ( H ) Representative immunoblots of YAP/TAZ and loading controls in nuclear and cytosolic lysates, accompanied by quantification of normalized nuclear TAZ expression and nuclear:cytosolic TAZ ratio, showing reduced nuclear TAZ in HUVEC over-expressing WT vs. K1003R IGF-1R. ns denotes non-specific band in α-tubulin blot. Data expressed as mean (SEM). * P < 0.05; n = 3, 3 in a–g and n = 4, 4 in h. All statistical comparisons are made with unpaired Student’s t -tests.
    Figure Legend Snippet: IGF-1 receptor over-expression reduces paracellular leakage and LDL-cholesterol uptake in human endothelial cells via its kinase domain. ( A ) Schema of lentiviral constructs used to achieve doxycycline-inducible WT or kinase-dead (K1003R) IGF-1R over-expression. ( B ) WT and K1003R IGF-1R protein expression are increased approximately three-fold by doxycycline. ( C ) Representative images of HUVEC VE-Cadherin with either WT or K1003R IGF-1R over-expression (VE-Cadherin—red, DAPI—blue). D ) VE-Cadherin junction thickness is reduced in confluent HUVEC exposed to 100 μM hydrogen peroxide over-expressing WT IGF-1R, but remains unchanged with cells over-expressing K1003R IGF-1R. ( E ) VE-Cadherin junction area is similar in confluent HUVEC over-expressing WT or K1003R IGF-1R. ( F ) Paracellular leakage of 40 kDa FITC-Dextran is reduced in HUVEC over-expressing WT IGF-1R, but not K1003R, IGF-1R. G ) Uptake of BODIPY-labelled LDL-cholesterol is reduced in HUVEC over-expressing WT IGF-1R, but not K1003R, IGF-1R (representative images on left; BODIPY—green, DAPI—blue). ( H ) Representative immunoblots of YAP/TAZ and loading controls in nuclear and cytosolic lysates, accompanied by quantification of normalized nuclear TAZ expression and nuclear:cytosolic TAZ ratio, showing reduced nuclear TAZ in HUVEC over-expressing WT vs. K1003R IGF-1R. ns denotes non-specific band in α-tubulin blot. Data expressed as mean (SEM). * P < 0.05; n = 3, 3 in a–g and n = 4, 4 in h. All statistical comparisons are made with unpaired Student’s t -tests.

    Techniques Used: Over Expression, Construct, Expressing, Western Blot



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    IGF-1 receptor over-expression reduces paracellular leakage and LDL-cholesterol uptake in human endothelial cells via its kinase domain. ( A ) Schema of lentiviral constructs used to achieve doxycycline-inducible WT or kinase-dead (K1003R) IGF-1R over-expression. ( B ) WT and K1003R IGF-1R protein expression are increased approximately three-fold by doxycycline. ( C ) Representative images of <t>HUVEC</t> VE-Cadherin with either WT or K1003R IGF-1R over-expression (VE-Cadherin—red, DAPI—blue). D ) VE-Cadherin junction thickness is reduced in confluent HUVEC exposed to 100 μM hydrogen peroxide over-expressing WT IGF-1R, but remains unchanged with cells over-expressing K1003R IGF-1R. ( E ) VE-Cadherin junction area is similar in confluent HUVEC over-expressing WT or K1003R IGF-1R. ( F ) Paracellular leakage of 40 kDa FITC-Dextran is reduced in HUVEC over-expressing WT IGF-1R, but not K1003R, IGF-1R. G ) Uptake of BODIPY-labelled LDL-cholesterol is reduced in HUVEC over-expressing WT IGF-1R, but not K1003R, IGF-1R (representative images on left; BODIPY—green, DAPI—blue). ( H ) Representative immunoblots of YAP/TAZ and loading controls in nuclear and cytosolic lysates, accompanied by quantification of normalized nuclear TAZ expression and nuclear:cytosolic TAZ ratio, showing reduced nuclear TAZ in HUVEC over-expressing WT vs. K1003R IGF-1R. ns denotes non-specific band in α-tubulin blot. Data expressed as mean (SEM). * P < 0.05; n = 3, 3 in a–g and n = 4, 4 in h. All statistical comparisons are made with unpaired Student’s t -tests.
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    IGF-1 receptor over-expression reduces paracellular leakage and LDL-cholesterol uptake in human endothelial cells via its kinase domain. ( A ) Schema of lentiviral constructs used to achieve doxycycline-inducible WT or kinase-dead (K1003R) IGF-1R over-expression. ( B ) WT and K1003R IGF-1R protein expression are increased approximately three-fold by doxycycline. ( C ) Representative images of <t>HUVEC</t> VE-Cadherin with either WT or K1003R IGF-1R over-expression (VE-Cadherin—red, DAPI—blue). D ) VE-Cadherin junction thickness is reduced in confluent HUVEC exposed to 100 μM hydrogen peroxide over-expressing WT IGF-1R, but remains unchanged with cells over-expressing K1003R IGF-1R. ( E ) VE-Cadherin junction area is similar in confluent HUVEC over-expressing WT or K1003R IGF-1R. ( F ) Paracellular leakage of 40 kDa FITC-Dextran is reduced in HUVEC over-expressing WT IGF-1R, but not K1003R, IGF-1R. G ) Uptake of BODIPY-labelled LDL-cholesterol is reduced in HUVEC over-expressing WT IGF-1R, but not K1003R, IGF-1R (representative images on left; BODIPY—green, DAPI—blue). ( H ) Representative immunoblots of YAP/TAZ and loading controls in nuclear and cytosolic lysates, accompanied by quantification of normalized nuclear TAZ expression and nuclear:cytosolic TAZ ratio, showing reduced nuclear TAZ in HUVEC over-expressing WT vs. K1003R IGF-1R. ns denotes non-specific band in α-tubulin blot. Data expressed as mean (SEM). * P < 0.05; n = 3, 3 in a–g and n = 4, 4 in h. All statistical comparisons are made with unpaired Student’s t -tests.
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    Image Search Results


    IGF-1 receptor over-expression reduces paracellular leakage and LDL-cholesterol uptake in human endothelial cells via its kinase domain. ( A ) Schema of lentiviral constructs used to achieve doxycycline-inducible WT or kinase-dead (K1003R) IGF-1R over-expression. ( B ) WT and K1003R IGF-1R protein expression are increased approximately three-fold by doxycycline. ( C ) Representative images of HUVEC VE-Cadherin with either WT or K1003R IGF-1R over-expression (VE-Cadherin—red, DAPI—blue). D ) VE-Cadherin junction thickness is reduced in confluent HUVEC exposed to 100 μM hydrogen peroxide over-expressing WT IGF-1R, but remains unchanged with cells over-expressing K1003R IGF-1R. ( E ) VE-Cadherin junction area is similar in confluent HUVEC over-expressing WT or K1003R IGF-1R. ( F ) Paracellular leakage of 40 kDa FITC-Dextran is reduced in HUVEC over-expressing WT IGF-1R, but not K1003R, IGF-1R. G ) Uptake of BODIPY-labelled LDL-cholesterol is reduced in HUVEC over-expressing WT IGF-1R, but not K1003R, IGF-1R (representative images on left; BODIPY—green, DAPI—blue). ( H ) Representative immunoblots of YAP/TAZ and loading controls in nuclear and cytosolic lysates, accompanied by quantification of normalized nuclear TAZ expression and nuclear:cytosolic TAZ ratio, showing reduced nuclear TAZ in HUVEC over-expressing WT vs. K1003R IGF-1R. ns denotes non-specific band in α-tubulin blot. Data expressed as mean (SEM). * P < 0.05; n = 3, 3 in a–g and n = 4, 4 in h. All statistical comparisons are made with unpaired Student’s t -tests.

    Journal: Cardiovascular Research

    Article Title: Endothelial insulin-like growth factor-1 signalling regulates vascular barrier function and atherogenesis

    doi: 10.1093/cvr/cvaf055

    Figure Lengend Snippet: IGF-1 receptor over-expression reduces paracellular leakage and LDL-cholesterol uptake in human endothelial cells via its kinase domain. ( A ) Schema of lentiviral constructs used to achieve doxycycline-inducible WT or kinase-dead (K1003R) IGF-1R over-expression. ( B ) WT and K1003R IGF-1R protein expression are increased approximately three-fold by doxycycline. ( C ) Representative images of HUVEC VE-Cadherin with either WT or K1003R IGF-1R over-expression (VE-Cadherin—red, DAPI—blue). D ) VE-Cadherin junction thickness is reduced in confluent HUVEC exposed to 100 μM hydrogen peroxide over-expressing WT IGF-1R, but remains unchanged with cells over-expressing K1003R IGF-1R. ( E ) VE-Cadherin junction area is similar in confluent HUVEC over-expressing WT or K1003R IGF-1R. ( F ) Paracellular leakage of 40 kDa FITC-Dextran is reduced in HUVEC over-expressing WT IGF-1R, but not K1003R, IGF-1R. G ) Uptake of BODIPY-labelled LDL-cholesterol is reduced in HUVEC over-expressing WT IGF-1R, but not K1003R, IGF-1R (representative images on left; BODIPY—green, DAPI—blue). ( H ) Representative immunoblots of YAP/TAZ and loading controls in nuclear and cytosolic lysates, accompanied by quantification of normalized nuclear TAZ expression and nuclear:cytosolic TAZ ratio, showing reduced nuclear TAZ in HUVEC over-expressing WT vs. K1003R IGF-1R. ns denotes non-specific band in α-tubulin blot. Data expressed as mean (SEM). * P < 0.05; n = 3, 3 in a–g and n = 4, 4 in h. All statistical comparisons are made with unpaired Student’s t -tests.

    Article Snippet: Passage 3–4 HUVEC (PromoCell) from at least three different donors were cultured in Endothelial Cell Growth Medium 2 (PromoCell) supplemented with 1× Antibiotic Antimycotic Solution (Merck) at 37°C in 5% CO 2 .

    Techniques: Over Expression, Construct, Expressing, Western Blot