GW29-e0091 miR-19a may participate in the mechanism of ac
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RESULTS HG-HF inhibited TRPV1 express ion in C MECs, and such
reduction was able to decrease Ca
2þ
content. T2DM signifi cant ly
impaired cardiac function, reduced glucose uptake, and damaged the
microvascular barrier, which was further aggravated by TRPV1
knockout. Exposure to HG-HF, p articularly in CMECs of TRPV 1
-/-
,give
rise to a higher level of apoptosis and a lower level of nitric oxide
production in the survived CMECs. Moreover, HG-HF markedly
enhanced generation of reactive oxygen species (ROS) and nitro-
tyrosine, especially in the absence of TR PV1. In addition, the admin-
istration of H
2
O
2
obviously reduced TRPV1 expression in CMECs.
More importantly, HG-HF significantly inhibited the expression of
peroxisome proliferator-activated receptor-
g
coactivator-1
a
(PGC-1
a
)
and optic atrophy 1 (OPA1) by reducing c ellular Ca
2þ
content, w hereas
OPA1 supplementation partly rev ersed the detrimental effects
induced by TRPV1 deficiency. Furthermore, long-term treatment of
capsaicin not only attenuated HG-HF-induced CMECs injury, but also
mitigated T2DM-in duced cardiac microvascular injury.
CONCLUSIONS T2DM gives rise to cardiac microvascular injury via
exacerbating the vicious cycle of TRPV1 blockage a nd ROS overload.
Prolonged dietary of capsaicin ca n protect cardiac microvessels
against T2DM by activa ting TRPV1/PGC-1
a
/OPA1 signaling mediated
suppression of oxidative/nitrative stress in CMECs.
GW29-e0076
Tom70 ameliorates cardiac microvascular injury induced by
diabetes combined with hyperlipidemia via inhibiting oxidative
stress
Juanni Hou, Yuxue Yang, Zhiping Song, Haifeng Pei
Chengdu Military Genera l Hospital
OBJECTIVES Cardiac microvascular injury, which is aggravated by
dyslipidemia, has a serious impact on cardia c circulatory balance and
physiological function. Besides several protective roles in cardiopathy,
the f unction of Tom70 ( translocase of the outer mitochondrial mem-
brane 70, Tom70) in cardiac microvessels is not well-defined. This
study was designed to determine the role of Tom70 in cardiac micro-
vascular endothelial cells (CMECs) in type 2 diabetes mellitus (T2DM).
METHODS T2DM-mice were es tablished by multiple injections of low-
dose streptozotocin and high-fat feeding. Cohorts of diabetic mice
received a 24-we ek treatm ent of metformin. CMECs were isolated and
cultured with norma l glucose (NG, 5.5 mmol/L), high glucose (HG,
25 mmo1/L) medium, and HG plus high fat ( HG-HF, the high-fat con-
centration was 500
m
mol/L).
RESULTS T2DM impaired cardiac function, disturbed glucose-uptake,
damaged m icrovascular integrity, and promoted myoca rdial fibrosis.
Exposure to HG-HF led to a higher level of apoptosis and a lower level
of nitric oxide production in viable CMECs. HG-HF markedly enhanced
generation of reactive oxygen species (ROS) and malondialdehyde. HG-
HF further worse n mitochondrial function and depre ssed Tom70
expression. In contrast, Tom70-upregulation partly reversed these
detrimental effects induced by HG-HF. Furthermore, long-time treat-
ment of me tformin not only mitigat ed cardiac microvascular injury
caused by T2D M, but also attenuated CMECs injury induced by HG-HF,
which were interrupted after Tom70 knocked down.
CONCLUSIONS T2DM leads to cardiac microvascular injury by vicious
circle of Tom70 decline, mitochondrial dysfunction, and ROS overload
in CMECs. Prolonged consumption of metformin can promote Tom70
and suppress oxidative stress. Collectively, our data reveal a new role
of Tom70 in CMECs, providing a novel ta rget of metformin for cardiac
microvascular protection.
GW29-e0080
TheprotectiveroleofAsprosinagainstdiabetesin
cardiomyocytes
Jian Feng,
1
Yuxue Yang,
2
Yongjian Yang,
1
Haifeng Pei
1
1
Chengdu Military General Hospital;
2
Southwest Jiaotong
University School of Medici ne Che n g du
OBJECTIVES Diabetic cardi omyopathy (DCM) is one of the most
important independent complications of diabetes mellitus, which
oftenleadtolater-periodheartfailureanddeath.Asprosinisanew
endogenous small molecular protein that plays an important role in
glycolipid metabolism. However, informatio n regarding the role of
Asprosin in DCM remains unavailable. Via conducting a hospital-
based study, we p urposed to ascertain the potential relations hip
between circulating asprosin concentrations and DCM. Then , in order
to find whether Asprosin have impact on apoptosis of mouse
cardiomyocytes (MCMs) induced by hyperglycemia, we conduct the
experiment in vivo and vitro.
METHODS In clinical, 22 patients with n ewly diagnosed type 2 dia-
betes (T2DM) were screened, matched w ith same healthy volunteers.
In v ivo, C57BL6/J mice were randomly divided into control group
(n¼20) and T2DM group (n¼20). Control mice were fed by normal diet
with intraperitoneal injection of citrate buffer, and T2DM mice were
adopted high fat diet and streptozotocin injection. In vitro,MCMs
were assigned into normal glucose group (NG, 5.5 mM) and high
glucose group (HG,33 mM).
RESULTS The clinical study revealed that the plasma levels of
Asprosin were significantly increa sed in diabetes compared with the
healthy volunteers (P<0.05). The level of Asprosin in T2DM mouse
showed a consistent trend ( P<0.05). Besides, in vitro,theapoptosisin
HG ,group was significantly increased (P<0.01), while Asprosin
intervention could remarkably rescue these apoptotic cells ( P<0.05).
Meanwhile, under the same high glucose condition, Asprosin could
decrease the generation of MDA and ROS in MCMs dramaticall y
(P<0.05). However, H
2
O
2
, a particularly efficien t oxidant, could block
the protective effect of Asprosin (P<0.05).
CONCLUSIONS The increase of plasma Asprosin can significantly
reduce high glucose-induced cardiomyocytes apoptosis, which may
be a kind of self-protection mechanism for diabetic cardiomyopathy.
GW29-e0082
Chronic Intermittent Hypoxia Induces Endothelial Insulin
Resistance in vivo and in vitro
Linyi Li, Yunyun Yang, Huina zhang, Xinliang Ma,
Yanwen Qin, Yongxiang Wei
Beijing Inst of Heart, Lung and Blood Vessel Disea ses, Beijing, China
OBJECTIVES Obstructive sleep apnea, a condition leading to c hronic
intermittent hypoxia (CIH), is an independent risk factor for cardio-
vascular disease and type 2 diabetes and is correlated with insulin
resistance. Insulin stimulates production of nitric oxide (NO) in
vascular endothelial cells throug h the IRS-1/PI3K/Akt/eNOS pathway
(IRS-1, insulin receptor substrate 1; PI3K, phos phatidylinositol 3-ki-
nase; eNOS, endothelial NO synthase). Endothelial cells directly
expose to blood flow and respond to oxygen concentration change in
flow. We wondered if and how CIH would affect insulin signalling/
action in endothelial cells.
METHODS C57BL/6J mice were exposed to CIH (2 1%-5%, 90 s/cycle, 10
h/day) or interm ittent air for 7 week s. HUVECs were exposed to CIH
(21%-5%, 1 h/cycle) for 24 h or 48 h with or without insulin.
RESULTS We observed that CIH increased systolic blood pressure and
impaired endothelium-dependent relaxation of aortas in C57BL/6J
mice. CIH increased IR S-1 phosphorylation at Ser307 and Ser612 and
impaired insulin-stimulated phosphor ylati on of IR S-1 at Tyr896 and
Akt/eNOS pathway in aortas. Furthermore, CIH activated hypoxia-
inducible factor 1
a
(HIF-1
a
) and nuclear factor kappa B (NF-
k
B) in
aortas. In vitro, C IH activated e ndothelial HIF-1
a
signaling, impaired
endothelial insulin signaling and reduced insulin-mediated NO pro-
duction. I n addition, C IH resulted in mitochondria proton leak and
elevated oxygen consumption in HUVECs. Increased oxygen con-
sumption further leaded to endothelial hypoxia and HIF-1
a
induction.
Pharmacological inhibition of proton leak ameliorated CIH-induced
endothelial insulin resistance in HUVECs.
CONCLUSIONS Our data suggest that CIH induces insulin resistant
endothelial dysfunction, which may be associated with HIF-1
a
in-
duction and proton leak.
GW29-e0091
miR-19a may participate in the mechanism of acute myocardial
infarction by targeting LDL receptor related protein 2
Wenjiang Chen,
1,2
Can Chen
2
1
The Cardiovascular department of the Second Af fi liate d Hospital of
Chongqing Medical University;
2
The Cardiovascular department of the
Affiliated Hospital of Guangdong Medical University
OBJECTIVES To study the mechanism and the relationship of the LDL
receptor related protein 2(LRP2) and miR-19a in acute myocardial
infarction (AMI).
METHODS 45 AMI cases were enrolled as AMI group, and 45 stable
chronic coronary artery disease (SCAD) cases wer e recruited as contro l
group. Plasma miR-19a was de tected by qRT-PCR, and miR-19a related
ncRNAs (miRNAs, lncRNAs, circRNAs) and their functions were
C2
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, VOL. 72, NO. 16, SUPPL C, 2018
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