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      <firstAuthor>Babay, Imre</firstAuthor>
      <title>SYSTEMIC INFLAMMATION INDUCED BY ANGIOTENSIN II INCREASES C3a-MEDIATED VASOCONSTRICTION IN MICE</title>
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      <abstractText>Introduc�on: Cardiovascular diseases are known to be associated with ac�va�on of 
the complement system, however, the precise rela�onship between the two processes is 
partly unclear. The complement component C3a receptor (C3aR) has been iden�fied in various 
cell types within the mouse arterial wall and the vasoconstrictor effect of C3a may be mediated 
by resident macrophages in the adven��a via thromboxane A2 (TXA2) release, as found by our 
workgroup in previous research.
Aims: The primary objec�ve of this study was to determine the effects of chronic 
angiotensin II (Ang II) administra�on on C3a-induced vasoconstric�on in mice, along with 
demonstra�ng the presence of macrophages in the adven��a using alterna�ve methods.
Methods: Changes in the isometric tension of the vascular segments were measured 
using myography a�er isola�ng thoracic and abdominal aor�c segments of adult male C57BL/6 
mice. The mice were infused with either Ang II (520 ng/kg/min) or saline for 14 days via microosmo�c pumps implanted in the subscapular region. qPCR assays were performed to measure 
the expression level of C3aR and the mouse macrophage marker F4/80. The expression of 
other genes involved in the signaling pathway, such as Cyclooxygenase 1 and 2 (Cox1 and 
Cox2), thromboxane A synthase 1 (Tbxas1), and thromboxane A2 receptor (Tbxa2r), were 
inves�gated. The localiza�on of C3AR1 was confirmed using immunohistochemistry. The 
mechanism of the contrac�on was examined using the cyclooxygenase (COX) inhibitor 
indomethacin and SQ29548, a thromboxane prostanoid (TP) receptor antagonist.
Results: An increased response to C3a (63–77) was observed in the vascular segments 
due to the increased expression of C3aR caused by Ang II treatment compared to controls that 
received saline infusion. The qPCR results revealed an increase in the expression of F4/80 and 
C3aR in the aortas, par�cularly in the adven��a, due to Ang II infusion. A�er removing the 
endothelium, the vasoconstric�on increased, while the vessels became unresponsive to C3a 
a�er the administra�on of COX and TP receptor inhibitors and the removal of the adven��a.
Conclusion: It can be concluded from our results that chronic Ang II administra�on can 
lead to an enhanced vasoconstrictor response to C3a and an increased expression of C3aR in 
the aor�c wall, par�cularly in the adven��a where macrophages accumulate. Our findings 
propose that the vasoconstric�on induced by C3a in the mouse aorta is facilitated by 
macrophages that have gathered in the adven��a. During the development of various 
cardiovascular diseases, the effects of anaphylatoxins could be amplified and may contribute 
to the progression of the diseases</abstractText>
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      <label>Babay Imre et al. SYSTEMIC INFLAMMATION INDUCED BY ANGIOTENSIN II INCREASES C3a-MEDIATED VASOCONSTRICTION IN MICE. (2023)</label><template>&lt;div class=&quot;PublicationOther Publication short-list&quot;&gt; &lt;div class=&quot;authors&quot;&gt; &lt;span class=&quot;author-name&quot; mtid=&quot;10080442&quot;&gt; &lt;a href=&quot;/gui2/?type=authors&amp;mode=browse&amp;sel=10080442&quot; target=&quot;_blank&quot;&gt;Babay, Imre&lt;/a&gt; &lt;/span&gt; &lt;span class=&quot;author-type&quot;&gt; &lt;/span&gt; ; &lt;span class=&quot;author-name&quot; mtid=&quot;10069772&quot;&gt; &lt;a href=&quot;/gui2/?type=authors&amp;mode=browse&amp;sel=10069772&quot; target=&quot;_blank&quot;&gt;Melinda Kerkovits, Nóra&lt;/a&gt; &lt;/span&gt; &lt;span class=&quot;author-type&quot;&gt; &lt;/span&gt; ; &lt;span class=&quot;author-name&quot; mtid=&quot;10086970&quot;&gt; &lt;a href=&quot;/gui2/?type=authors&amp;mode=browse&amp;sel=10086970&quot; target=&quot;_blank&quot;&gt;Virág Tóth, Csillag&lt;/a&gt; &lt;/span&gt; &lt;span class=&quot;author-type&quot;&gt; &lt;/span&gt; ; &lt;span class=&quot;author-name&quot; mtid=&quot;10027489&quot;&gt; &lt;a href=&quot;/gui2/?type=authors&amp;mode=browse&amp;sel=10027489&quot; target=&quot;_blank&quot;&gt;Szénási, Gábor&lt;/a&gt; &lt;/span&gt; &lt;span class=&quot;author-type&quot;&gt; &lt;/span&gt; ; &lt;span class=&quot;author-name&quot; mtid=&quot;10020915&quot;&gt; &lt;a href=&quot;/gui2/?type=authors&amp;mode=browse&amp;sel=10020915&quot; target=&quot;_blank&quot;&gt;Kosztelnik, Mónika&lt;/a&gt; &lt;/span&gt; &lt;span class=&quot;author-type&quot;&gt; &lt;/span&gt; ; &lt;span class=&quot;author-name&quot; mtid=&quot;10009921&quot;&gt; &lt;a href=&quot;/gui2/?type=authors&amp;mode=browse&amp;sel=10009921&quot; target=&quot;_blank&quot;&gt;Benyó, Zoltán&lt;/a&gt; &lt;/span&gt; &lt;span class=&quot;author-type&quot;&gt; &lt;/span&gt; &lt;/div &gt; &lt;div class=&quot;title&quot;&gt;&lt;a href=&quot;/gui2/?mode=browse&amp;params=publication;34747676&quot; mtid=&quot;34747676&quot; target=&quot;_blank&quot;&gt;SYSTEMIC INFLAMMATION INDUCED BY ANGIOTENSIN II INCREASES C3a-MEDIATED VASOCONSTRICTION IN MICE&lt;/a&gt; &lt;span class=&quot;page&quot;&gt; pp. 189-189. , 1 p. &lt;/span&gt; (2023) &lt;/div&gt; &lt;div class=&quot;pub-info&quot;&gt; &lt;/div&gt; &lt;div class=&quot;pub-end&quot;&gt;&lt;div class=&quot;identifier-list&quot;&gt; &lt;span class=&quot;identifiers&quot;&gt; &lt;/span&gt; &lt;/div&gt; &lt;div class=&quot;short-pub-prop-list&quot;&gt; &lt;span class=&quot;short-pub-mtid&quot;&gt; Közlemény:34747676 &lt;/span&gt; &lt;span class=&quot;status-holder&quot;&gt;&lt;span class=&quot;status-data status-ADMIN_APPROVED&quot;&gt; Admin láttamozott &lt;/span&gt;&lt;/span&gt; &lt;span class=&quot;pub-core&quot;&gt;Forrás &lt;/span&gt; &lt;span class=&quot;pub-type&quot;&gt;Egyéb (Nem besorolt ) &lt;/span&gt; &lt;!-- &amp;&amp; !record.category.scientific --&gt; &lt;span class=&quot;pub-category&quot;&gt;Tudományos&lt;/span&gt; &lt;/div&gt; &lt;/div&gt; &lt;/div&gt;</template><template2>&lt;div class=&quot;PublicationOther Publication long-list&quot;&gt; &lt;div class=&quot;authors&quot;&gt; &lt;img title=&quot;Forrásközlemény&quot; style=&quot;float: left&quot; src=&quot;/frontend/resources/grid/publication-core-icon.png&quot;&gt; &lt;div class=&quot;autype autype0&quot;&gt; &lt;span class=&quot;author-name&quot; mtid=&quot;10080442&quot;&gt;&lt;a href=&quot;/gui2/?type=authors&amp;mode=browse&amp;sel=10080442&quot; target=&quot;_blank&quot;&gt;Babay Imre (&lt;span class=&quot;authorship-author-name&quot;&gt;Babay Imre&lt;/span&gt; &lt;span class=&quot;authorAux-mtmt&quot;&gt; élettan, kórélettan&lt;/span&gt;) &lt;/a&gt; &lt;/span&gt; &lt;span class=&quot;author-affil&quot;&gt;&lt;span title=&quot;Semmelweis Egyetem&quot;&gt;SE&lt;/span&gt;/&lt;span title=&quot;Általános Orvostudományi Kar&quot;&gt;AOK&lt;/span&gt;/&lt;span title=&quot;Intézet&quot;&gt;I&lt;/span&gt;/Transzlációs Medicina Intézet&lt;/span&gt; ;&amp;nbsp;&amp;nbsp;&amp;nbsp; &lt;span class=&quot;author-name&quot; mtid=&quot;10069772&quot;&gt;&lt;a href=&quot;/gui2/?type=authors&amp;mode=browse&amp;sel=10069772&quot; target=&quot;_blank&quot;&gt;Melinda Kerkovits Nóra (&lt;span class=&quot;authorship-author-name&quot;&gt;Kerkovits Nóra Melinda&lt;/span&gt; &lt;span class=&quot;authorAux-mtmt&quot;&gt; Élettan&lt;/span&gt;) &lt;/a&gt; &lt;/span&gt; &lt;span class=&quot;author-affil&quot;&gt;&lt;span title=&quot;Semmelweis Egyetem&quot;&gt;SE&lt;/span&gt;/&lt;span title=&quot;Általános Orvostudományi Kar&quot;&gt;AOK&lt;/span&gt;/&lt;span title=&quot;Intézet&quot;&gt;I&lt;/span&gt;/Transzlációs Medicina Intézet&lt;/span&gt; ;&amp;nbsp;&amp;nbsp;&amp;nbsp; &lt;span class=&quot;author-name&quot; mtid=&quot;10086970&quot;&gt;&lt;a href=&quot;/gui2/?type=authors&amp;mode=browse&amp;sel=10086970&quot; target=&quot;_blank&quot;&gt;Virág Tóth Csillag (&lt;span class=&quot;authorship-author-name&quot;&gt;Tóth Csillag Virág&lt;/span&gt; &lt;span class=&quot;authorAux-mtmt&quot;&gt; élettan, kórélettan&lt;/span&gt;) &lt;/a&gt; &lt;/span&gt; &lt;span class=&quot;author-affil&quot;&gt;&lt;span title=&quot;Semmelweis Egyetem&quot;&gt;SE&lt;/span&gt;/&lt;span title=&quot;Általános Orvostudományi Kar&quot;&gt;AOK&lt;/span&gt;/&lt;span title=&quot;Intézet&quot;&gt;I&lt;/span&gt;/Transzlációs Medicina Intézet&lt;/span&gt; ;&amp;nbsp;&amp;nbsp;&amp;nbsp; &lt;span class=&quot;author-name&quot; mtid=&quot;10027489&quot;&gt;&lt;a href=&quot;/gui2/?type=authors&amp;mode=browse&amp;sel=10027489&quot; target=&quot;_blank&quot;&gt;Szénási Gábor (&lt;span class=&quot;authorship-author-name&quot;&gt;Szénási Gábor&lt;/span&gt; &lt;span class=&quot;authorAux-mtmt&quot;&gt; kórélettan&lt;/span&gt;) &lt;/a&gt; &lt;/span&gt; &lt;span class=&quot;author-affil&quot;&gt;&lt;span title=&quot;Semmelweis Egyetem&quot;&gt;SE&lt;/span&gt;/&lt;span title=&quot;Általános Orvostudományi Kar&quot;&gt;AOK&lt;/span&gt;/&lt;span title=&quot;Intézet&quot;&gt;I&lt;/span&gt;/Transzlációs Medicina Intézet&lt;/span&gt; ;&amp;nbsp;&amp;nbsp;&amp;nbsp; &lt;span class=&quot;author-name&quot; mtid=&quot;10020915&quot;&gt;&lt;a href=&quot;/gui2/?type=authors&amp;mode=browse&amp;sel=10020915&quot; target=&quot;_blank&quot;&gt;Kosztelnik Mónika (&lt;span class=&quot;authorship-author-name&quot;&gt;Kosztelnik Mónika&lt;/span&gt; &lt;span class=&quot;authorAux-mtmt&quot;&gt; Genetika&lt;/span&gt;) &lt;/a&gt; &lt;/span&gt; &lt;span class=&quot;author-affil&quot;&gt;&lt;span title=&quot;Semmelweis Egyetem&quot;&gt;SE&lt;/span&gt;/&lt;span title=&quot;Általános Orvostudományi Kar&quot;&gt;AOK&lt;/span&gt;/&lt;span title=&quot;Intézet&quot;&gt;I&lt;/span&gt;/Transzlációs Medicina Intézet; &lt;span title=&quot;Semmelweis Egyetem&quot;&gt;SE&lt;/span&gt;/&lt;span title=&quot;Általános Orvostudományi Kar&quot;&gt;AOK&lt;/span&gt;/&lt;span title=&quot;Intézet&quot;&gt;I&lt;/span&gt;/&lt;span title=&quot;Transzlációs Medicina Intézet&quot;&gt;TMI&lt;/span&gt;/ELKH-SE Cerebrovaszkuláris és Neurokognitív Betegségek Kutatócsoport&lt;/span&gt; ;&amp;nbsp;&amp;nbsp;&amp;nbsp; &lt;span class=&quot;author-name&quot; mtid=&quot;10009921&quot;&gt;&lt;a href=&quot;/gui2/?type=authors&amp;mode=browse&amp;sel=10009921&quot; target=&quot;_blank&quot;&gt;Benyó Zoltán (&lt;span class=&quot;authorship-author-name&quot;&gt;Benyó Zoltán&lt;/span&gt; &lt;span class=&quot;authorAux-mtmt&quot;&gt; Élettan és kórélettan&lt;/span&gt;) &lt;/a&gt; &lt;/span&gt; &lt;span class=&quot;author-affil&quot;&gt;&lt;span title=&quot;Semmelweis Egyetem&quot;&gt;SE&lt;/span&gt;/&lt;span title=&quot;Általános Orvostudományi Kar&quot;&gt;AOK&lt;/span&gt;/&lt;span title=&quot;Intézet&quot;&gt;I&lt;/span&gt;/Transzlációs Medicina Intézet; &lt;span title=&quot;Semmelweis Egyetem&quot;&gt;SE&lt;/span&gt;/&lt;span title=&quot;Általános Orvostudományi Kar&quot;&gt;AOK&lt;/span&gt;/&lt;span title=&quot;Intézet&quot;&gt;I&lt;/span&gt;/&lt;span title=&quot;Transzlációs Medicina Intézet&quot;&gt;TMI&lt;/span&gt;/ELKH-SE Cerebrovaszkuláris és Neurokognitív Betegségek Kutatócsoport&lt;/span&gt; &lt;/div&gt; &lt;/div&gt; &lt;div class=&quot;title&quot;&gt;&lt;a href=&quot;/gui2/?mode=browse&amp;params=publication;34747676&quot; target=&quot;_blank&quot;&gt;SYSTEMIC INFLAMMATION INDUCED BY ANGIOTENSIN II INCREASES C3a-MEDIATED VASOCONSTRICTION IN MICE&lt;/a&gt;&lt;/div&gt; &lt;div class=&quot;description&quot;&gt; &lt;/div&gt; &lt;div class=&quot;country&quot;&gt; Megjelenés: &lt;span class=&quot;pageLength&quot;&gt;1 p.&lt;/span&gt; &lt;span class=&quot;publishedYear&quot;&gt;(2023)&lt;/span&gt; &lt;/div&gt; &lt;div class=&quot;pub-footer&quot;&gt; &lt;span class=&quot;language&quot; xmlns=&quot;http://www.w3.org/1999/html&quot;&gt;Nyelv: Angol &lt;/span&gt; &lt;span class=&quot;identifiers&quot;&gt; &lt;/span&gt; &lt;div class=&quot;mtid&quot;&gt;&lt;span class=&quot;long-pub-mtid&quot;&gt;Közlemény: 34747676&lt;/span&gt; | &lt;span class=&quot;status-data status-ADMIN_APPROVED&quot;&gt; Admin láttamozott &lt;/span&gt; Forrás | &lt;span class=&quot;type-subtype&quot;&gt;Egyéb ( Nem besorolt ) &lt;/span&gt; | &lt;span class=&quot;pub-category&quot;&gt;Tudományos&lt;/span&gt; | &lt;span class=&quot;publication-sourceOfData&quot;&gt;kézi felvitel&lt;/span&gt; &lt;/div&gt; &lt;div class=&quot;funder&quot;&gt; (K-125174) Támogató: OTKA, (K-135683) Támogató: OTKA, (K-139230) Támogató: NKFIH, (2020-1.1.6-JÖVŐ-2021-00010), Az orvos-, egészségtudományi- és gyógyszerészképzés tudományos műhelyeinek fejlesztése(EFOP-3.6.3-VEKOP-16-2017-00009) Támogató: EFOP-VEKOP, (TKP2021-EGA-25) &lt;/div&gt; &lt;div class=&quot;lastModified&quot;&gt;Utolsó módosítás: 2024.06.20. 09:50 Csajbók Edit (SE_KK_Admin5_CSE, admin) &lt;/div&gt; &lt;/div&gt;&lt;/div&gt;</template2>
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