自來文人每以漢賦與唐詩、宋詞、元曲分庭抗禮，各據一代之勝。 孫松友四六叢話言兩漢之賦「雖不盡傳，而沈博絕麗之作，至今膾炙，非後世所可及 」。王觀堂亦指此為一代文學，後世莫能繼焉。焦里堂則直指「魏晉以後之賦，為漢 賦之餘氣遊魂也。」是以為謀賦體之正本清源，遂決作漢賦之研究。 然漢賦多矣。若一一推求，勢所難能。今僅就其代表作家加以探索，考兩漢最具代表 性之賦家，厥惟揚馬，後世雖有益以班張，合稱四傑者。然孟堅為史家之良材，平子 為科學之巨擘，其於賦也，並沐揚馬之遺澤，未能更樹一宗，故乃先取此二家，以資 辨析焉。 本文分七章，長卿子雲分論。以評傳居首，賦篇之分析次之，然後殿之以賦篇韻譜分 析。二家之評傳，皆分時代背景，生平評述、著述評介三節，乃先就文學流變、政治 情勢、社會經濟、學術思想各端而探究之，以為評斷其人品及作品之依據。然後考其 先世身家、平生略歷、予以先後，繫以年代，再就其學殖人品、思想主張、與文學地 位等各方面，加以考評。至於著述評介，則將分門別類，述介其內容，勾勒其體貌， 衡量其價值，以概見其成就。 若夫馬揚賦篇之分析，則各立專章，並依篇為節，論其結構，析其內容，究其技巧， 述其影響。此外並依各賦之性質，或定其題稱、辨其真偽；或考其動機、釐其主旨； 或探其體類，繹其思維，皆欲務求深入而詳盡。 賦篇韻譜之排列與辨析，旨在深究馬揚賦篇之體製形貌，明西漢之音韻，以及蜀郡方 音之影響，進而作為探究作品真偽之依據。 末章則在綜述馬揚二家辭賦之特色，並作比較研究。就其組織、修辭、內質、外象分 別考述，大體依友人黃春貴所撰文心雕龍創作論、分謀篇、章法、句式、字詞、比興 、夸飾、用典、隱秀、思想、情感、想像、氣力、辭采、聲律、對偶、風格等子目、 一一品較。 /

Made available in DSpace on 2014-12-17T15:06:47Z (GMT). No. of bitstreams: 1 ChristielenDS.pdf: 591277 bytes, checksum: c7d5644d2c09079d3ca05e8c502e6d39 (MD5) Previous issue date: 2009-11-25 / Coordena??o de Aperfei?oamento de Pessoal de N?vel Superior / Pygmalion (1913), by George Bernard Shaw (1856-1950), has many studies in literary criticism. However, this study brings a new interpretation to Shaw s play based on Harold Bloom s theory and methodology, that is, the anxiety of influence and the dialectic of revisionism. Through the analysis of poetic influence and the dialectic of love, we can see that Pygmalion represents an apophrades in relation to William Shakespeare s The Taming of the Shrew (1593) and Ovid s myth of Pygmalion and Galatea in Metamorphosis (c. 14), which creates a family romance between the three stories. Shaw s play surpasses The Taming of the Shrew when it shows the possibility of the relation between this parent poem and Ovid s myth, which it is also its parent poem, and because it represents a strong misreading of Shakespeare s play as well as of Ovid s myth. / Pigmale?o (Pygmalion, 1913), de George Bernard Shaw (1856-1950), possui uma grande fortuna cr?tica. Entretanto, o presente estudo oferece uma nova interpreta??o para a pe?a de Shaw, com base na teoria e metodologia do cr?tico norte- mericano Harold Bloom (1930- ), a saber, a ang?stia da influ?ncia e o revisionismo dial?tico. Atrav?s da an?lise da influ?ncia po?tica e da dial?tica do amor ? que se pode perceber que Pigmale?o representa uma apophrades em rela??o ? pe?a A megera domada (The Taming of the Shrew, 1593) de William Shakespeare (1564-1616) e ao mito de Pigmale?o e Galat?ia encontrado em Metamorfoses (c. 14) de Ov?dio (43 a.C.-17), formando um romance familiar entre as tr?s. A pe?a de Shaw supera seu poema pai (A megera domada) ao mostrar a possibilidade de rela??o deste com a hist?ria de Ov?dio (sendo assim seu poema pai) e por fazer uma desleitura forte n?o s? da obra de Shakespeare, como tamb?m do mito de Ov?dio.

Une augmentation de la concentration de l’angiotensine II (Ang II) contribue à la prolifération, la migration et l’hypertrophie des cellules musculaires lisses vasculaires (CMLVs) par l’activation des voies des mitogen-activated protein kinases (MAPK) et de la phosphoinositide 3-kinase (PI3K)/protéine kinase B (PKB/Akt). L’Ang II induit l’activation du facteur de transcription early growth response protein-1 (Egr-1) et sa suractivation est remarquée dans les lésions athérosclérotiques et les modèles animaux de lésions vasculaires. La régulation des facteurs de transcription est effectuée par des histones désacétylases (HDACs) qui désacétylent les lysines des histones et protéines non-histones. L’Ang II induit la phosphorylation et l’export nucléaire de la classe IIa des HDACs, particulièrement les HDAC5, et une augmentation de celles-ci est observée dans les maladies vasculaires. L’Ang II est un puissant activateur des voies des MAPK et de la PI3K/Akt, toutefois l’implication de ces voies dans la phosphorylation des HDAC5 et l’expression de l’Egr-1 dans les CMLVs reste inexplorée. Dans cette étude, l’Ang II a induit la phosphorylation des HDAC5 sur la sérine 498 dans les A10 CMLVs. Un blocage pharmacologique de l’extracellular signal-regulated kinase 1/2 (ERK1/2) par U0126 n’a montré aucun effet significatif sur la phosphorylation et l’exclusion nucléaire des HDAC5 induite par l’Ang II. Par contre, l’inhibition de la voie PI3K par wortmannin, de l’Akt par SC66 ou le knockdown de l’Akt par des petits ARN interférents (siRNA) a atténué la phosphorylation et l’export nucléaire des HDAC5 induits par l’Ang II. Par ailleurs, l’inhibition de l’Akt ou le knockdown de cette kinase a diminué l’expression de l’Egr-1 induite dans les CMLVs stimulées par l’Ang II. L’inhibition des HDACs de la classe IIa par MC1568 ou TMP-195 ou bien le knockdown des HDAC5 a diminué l’expression de l’Egr-1 induite par l’Ang II. De plus, le blocage de l’export nucléaire des HDAC5 par la leptomycine B ou la KPT-330 a empêché la localisation cytoplasmique des HDAC5 et a atténué l’expression de l’Egr-1 en réponse à une stimulation de l’Ang II. L’hypertrophie vasculaire induite par l’Ang II a pu être inhibée par la suppression de l’HDAC5 et l’Egr-1. En conclusion, l’Ang II induit la phosphorylation et l’exclusion nucléaire des HDAC5 par la voie PI3K/Akt et non celle de ERK1/2; de plus, l’Ang II induit l’expression de l’Egr-1 à l’aide des HDAC5 via la voie Akt contribuant ainsi à l’hypertrophie des CMLVs. / Elevated concentration of angiotensin II (Ang II) contributes to vascular smooth muscle cells (VSMCs) proliferation, migration and hypertrophy by the activation of the mitogen-activated protein kinases (MAPK) and phosphoinositide 3-kinase (PI3K)/protein kinase B (PKB/Akt) pathways. Ang II induced the expression of early growth response protein-1 (Egr-1), which is a transcription factor that is upregulated in atherosclerosis lesions and in animal models of vascular injuries. The activation or derepression of gene transcription is mediated by histone deacetylases (HDACs), which deacetylate lysine residues from histone and non-histones proteins. Ang II-induced the phosphorylation and nuclear export of class IIa HDACs, notably HDAC5, and its elevated activation is observed in vascular pathologies. Ang II is a potent activator of the MAPK and PI3K/Akt pathways, however their implication in the phosphorylation of HDAC5 and Egr-1 expression in VSMCs remain unexplored. In this study, Ang II-induced HDAC5 phosphorylation at serine 498 in A10 VSMCs and pharmacological blockade of the extracellular signal-regulated kinase 1/2 (ERK1/2) by U0126 did not affect the phosphorylation and nuclear exclusion of HDAC5 in response to Ang II. Whereas, pharmacological inhibition of the PI3K by wortmannin, Akt by SC66 or small interfering RNA (siRNA)-induced silencing of Akt attenuated Ang II-induced HDAC5 phosphorylation and its nuclear export. Furthermore, inhibition or knockdown of Akt suppressed Ang II-induced Egr-1 expression. In addition, the inhibition of class IIa HDAC5 by MC1568, TMP-195 or HDAC5 knockdown by siRNA reduced Ang II-induced Egr-1 expression. The blockade of the nuclear export of HDAC5 by leptomycin B or KPT-330 prevented the cytoplasmic localization of HDAC5 and attenuated the expression of Egr-1 by Ang II in VSMCs. Moreover, HDAC5 or Egr-1 depletion prevented Ang II-induced cell hypertrophy. In summary, Ang II-induced HDAC5 phosphorylation and its nuclear export is mediated by the PI3K/Akt and not the ERK1/2 pathway, in addition, Ang II-induced Egr-1 expression involves the implication of HDAC5 via the Akt pathway which subsequently leads to VSMC hypertrophy.

Insulin regulated aminopeptidase (IRAP) was first identified in fat and muscle cells where it is believed to regulate GLUT4 translocation. It has since been found to be behind a variety of functions, many not yet fully understood. Preliminary research from Monash University suggested that IRAP may play a role in cellular senescence. Senescence is a term that describes arrested cell division and is a tumor repressive mechanism. Senescent cells have been shown to secrete, among other things, the growth hormone TGFβ1, which in turn plays an important role in the cell differentiation of fibroblasts to myofibroblasts. The potential link between IRAP and senescence was the basis of this work. Senescent fibroblasts from three different passages (n=3) in the BJ3 cell-line were cultured and treated with different IRAP inhibitors; ANG-4, AL06 and HFI-419 which were all compared to an untreated control group. They were marked with a β-galactosidase stain, a senescent cellmarker, and imaged. The study demonstrated that the IRAP inhibitors led to a certain decrease in % of senescent cells compared to the control groups. However, this reduction was not considered statistically significant. Similarly, inhibition of the enzyme did not indicate any influence over the differentiation of the cells. The lack of effect could be due to chance based on the low number of sample size, or the condition of the cells used in the trial as they were partially immortalized BJ fibroblasts well beyond the passage of their intended use. In order to further demonstrate an association between IRAP and senescence, further trials are required. / Insulin reglerad aminopeptidas (IRAP) introducerades till en början som ett markörprotein. Man har sedan dess funnit att den står bakom en rad olika funktioner, många ännu inte  fullt klarlagda. Preliminär forskning från laboratoriet i Monash University tydde på att IRAP kan ha en koppling till senescerande fibroblaster. Senescence är en term som beskriver upphörd celldelning och är en tumörrepressiv mekanism. Senescerande celler har påvisats utsekrera bland annat tillväxthormonet TGFβ1, som i sin tur spelar en viktig roll i celldifferentieringenav fibroblaster till myofibroblaster. Den potentiella kopplingen mellan IRAP och senescence låg som grund till detta arbete. Senescerande fibroblaster från tre olika kulturer (n=3) i BJ3-cellinjen odlades och behandlades med olika IRAP-inhibitorer; ANG-4, AL06 och HFI-419 som alla jämfördes med en kontrollgrupp. Därefter markerades de med en β-galaktosidas-markör, en markör för senescerande celler, och mikroskoperades. Studien påvisade att IRAP-inhibitorerna ledde till en viss procentuell minskning av senescerande celler jämfört med kontrollgrupperna. Dock bedömdes inte denna minskning som statistiskt signifikant i studien. Likväl fann man ingen procentuell minskning av differentierade fibroblaster. Hypotetiskt sett skulle man vilja se att reduktionen av senescerande celler motsvarade en nedreglering av TGFβ1-proteiner. Eftersom närvaron av TGFβ1 tros spela en ledande roll i celldifferentiering till myofibroblastfenotypen, bör den procentuella mängden differentierade cellerna minska med inhibitorbehandlingarna. Den bristande påverkan av enzyminhibitionen kan bero på en rad olika faktorer. Cellerna som användes under försökets gång var väl bortom deras brukliga användningscykel. För att vidare påvisa ett potentiellt samband mellan IRAP och senescence behöver vidare försök utföras.

本研究旨在從俄國學者Mikhail Bakhtin（1895-1975）狂歡節語言與身體論述的觀點探討「抵抗如何可能？」的問題，並且以台灣當代女性主義小說家李昂於1999年出版的《自傳の小說》為主要的案例，重新思索和說明語言／意義的民主化（democratization）意涵與可能性。 有別於過去論述分析雖然言明語言／意義與政治社會之間並非單向的因果關係，而是相互影響、建構的辯證關係，但在實際進行案例分析時，卻較少著墨於語言如何「由下而上地」對象徵秩序進行意義的顛覆，本研究以Bakhtin對狂歡節語言與身體論述的說明，依序對抵抗的意涵、抵抗的可能性以及抵抗如何在文本中呈現，提出理論性的再詮釋。本研究發現，Bakhtin對於抵抗的想像，乃是一種在傳播／溝通與對話中，藉由特定語言形式而動員的意識形態鬥爭。積極而言，抵抗旨在透過言說主體的表述建構自己的意義系統；消極而言，抵抗至少具有解構他人意義系統的政治意圖。 然而，由於Bakhtin在狂歡節研究中，並未確實回應他企圖探討的「抵抗如何可能？」的問題。因此，本研究融入Laclau與Mouffe的「接合實踐」、Butler的「論述行動」與「身體展演」，從「形式層面」推敲Bakhtin在「眾聲喧嘩」對話模式中所暗示的政治機會，並對「抵抗如何可能？」提出具體的政治方案，包括：眾聲喧嘩的文本空間、對話與敵對關係中的再意義化、諧擬的身體展演、策略性的本質主義。本研究並且藉由對李昂情慾書寫中的抵抗策略進行「書寫形式的意識形態分析」，具體說明「抵抗如何可能？」的理論／概念架構。 本研究發現，李昂的情慾書寫呈現出「歷史書寫的性別化」與「性別論述的狂歡化」這兩個主要的特性。藉此，李昂一方面揭露了父權意識形態的意義生產邏輯，另一方面也藉由批判父權意識形態建構另類的意義系統或敵對／反對論述。從這點回過頭來再詮釋「抵抗如何可能？」的問題，本研究認為抵抗的可能性可說是在眾聲喧嘩或「弱敘事性」的文本空間中，藉由「接合實踐」動員由下而上的「論述行動」，並以「策略性的本質主義」此一政治方案建構霸權化論述的意識形態鬥爭過程；而「身體論述」所誇大展演出的敵對關係，則是最具渲染力也最為具體的例說。

<p>This study addresses the issue of how to convert peptides into drug-like non- peptides with retained biological activities at peptide receptors. Angiotensin II (Asp-Arg-Val-Tyr-Ile-His-Pro-Phe, Ang II) was used as a model peptide. </p><p>Knowledge of the bioactive conformations of endogenous peptides is invaluable for the conversion of peptides into less peptidic analogues. Effectively constrained cyclic analogues, with retained pharmacological activities, may provide valuable information about the bioactive conformations of the peptide in question. </p><p>This thesis describes the development of synthesis for a number of protected, aldehyde-functionalized building blocks for standard solid phase peptide synthesis, and their use for the preparation of cyclic peptide analogues. The effect of variations in the side-chain lengths of the building blocks, on the outcome of the cyclizations was studied. Incorporation of a building block derived from L-aspartic acid afforded bicyclization towards the C-terininal end of the peptide, while for the corresponding L-glutamic acid derived building block, N-terminal directed bicyclization was achieved. A building block derived from L-2-aminoadipic acid was exploited for monocyclization furnishing <i>cis-</i> and <i>trans-</i> vinyl sulfide bridged peptide analogues. </p><p>The described cyclization methods have been applied to the synthesis of a number of conformationally constrained Ang II analogues, for which the pharmacological properties have been evaluated. Two of the Ang II analogues synthesized displayed high affinities and full agonist activities at the AT₁ angiotensin receptor, and have proven to be useful tools in the search for the bioactive conformation of Ang II.</p>

This study addresses the issue of how to convert peptides into drug-like non- peptides with retained biological activities at peptide receptors. Angiotensin II (Asp-Arg-Val-Tyr-Ile-His-Pro-Phe, Ang II) was used as a model peptide. Knowledge of the bioactive conformations of endogenous peptides is invaluable for the conversion of peptides into less peptidic analogues. Effectively constrained cyclic analogues, with retained pharmacological activities, may provide valuable information about the bioactive conformations of the peptide in question. This thesis describes the development of synthesis for a number of protected, aldehyde-functionalized building blocks for standard solid phase peptide synthesis, and their use for the preparation of cyclic peptide analogues. The effect of variations in the side-chain lengths of the building blocks, on the outcome of the cyclizations was studied. Incorporation of a building block derived from L-aspartic acid afforded bicyclization towards the C-terininal end of the peptide, while for the corresponding L-glutamic acid derived building block, N-terminal directed bicyclization was achieved. A building block derived from L-2-aminoadipic acid was exploited for monocyclization furnishing cis- and trans- vinyl sulfide bridged peptide analogues. The described cyclization methods have been applied to the synthesis of a number of conformationally constrained Ang II analogues, for which the pharmacological properties have been evaluated. Two of the Ang II analogues synthesized displayed high affinities and full agonist activities at the AT1 angiotensin receptor, and have proven to be useful tools in the search for the bioactive conformation of Ang II.

一在彰明馬氏於東漢經學之地位：如馬氏所注諸經皆為古學，故為東漢古學之集大成 者，此其一；以其精於訓詁，實為後世所謂漢學派之大家，其其二；馬氏說經兼採緯 書及陰陽五行之說，乃附和時代之習尚也，此其三；其雜糅今古文之學，為鄭氏注經 融會今古文之先導，此其四；馬氏博通群經，郊氏偏注諸經，亦得馬氏之啟示，此其 五；其注經兼引群書，後世之注疏家遂並相效之，此其六；其說經歸本人事，以發經 義之微旨，繫儒道於不墜，此其七；其解經，驗諸史實，以證經義之不誣，此其八； 馬氏不囿於師法、家法，使後人能放手研經，而無所拘泥，開後世經學恢宏之局，此 其九。 二在明馬氏經學之源流：如易本費氏，書從西州杜林，詩傳毛氏，三禮、春秋多遵賈 逵、鄭眾，孝經從劉歆校定古文，論語則從古論。 三在明馬氏之生平：誦詩讀書，不可不知其人，故列作者生平年譜一章，以明馬氏年 里、才學、性格、仕宦、交遊、著述之大略。 四在分述馬氏訓釋各經之略例，及其要義，以明馬氏經學之梗概。 五在比較馬融、鄭玄、王肅三家經說之異同，以明鄭、王經學之淵源。 六在校輯馬氏經注佚文，以便學者參稽焉。 /

王氏之學，廣矣，大矣。今所論者，僅就其注經之言，加以考辨，重在明其經學之怕 歸，至其他撰著，則不與也。 王氏注經，太半簡明切要，平易近人，所惜者，好攻鄭氏，「強辯求勝」，如本傳云 ：「肅集聖證論，以譏玄短。」又家語序云：「鄭氏學行五十載矣，自肅成童，始志 於學，而學鄭氏學矣，然尋文責實，考其上下，義理不安，違錯者多，是以奪而易之 。」故後人每有微詞，今撰述其言，采薈眾說，是其是而非其非，苟有一言可述，則 據理申闡，使隱義彰明，苟有一字之失，亦循實責名，使名符其實。 本文之內容： 王氏注經，據史志所載，為數甚繁，惜多已亡佚，今可見諸古籍所引，及各家所輯文 之成帙者，有周易注、尚書注、詩注、三禮注、左氏注、孝經注，論語注等七經，今 依唐陸德明經典釋文之序，列章申疏，亦所以借明經之次第也。 第一章：王肅之周易學。 第二章：王肅之周易學。 第三章：王肅之詩經學。 第四章：王肅之三禮學。 第五章：王肅之春秋左氏學。 第六章：王肅之孝經學。 第七章：王肅之論語學。 此外，前列結論，以為本文之喤引，並述及王肅之生平，家世，交遊及著述，取孟子 「知人論世」之義也。後列結論，作綜合之評述，借窺王氏注經態度及其影響。最後 附錄聖證論。王氏一家之經學，今可見者，庶盡於此矣。

L’athérosclérose est une pathologie cardiovasculaire chronique impliquant de nombreux acteurs. Les cellules du muscle lisse vasculaire (CMLV) jouent un important rôle dans la pathogénicité. Lors de la formation des plaques athérosclérotiques, ces cellules entraînent l’augmentation de la taille de l’athérome, accentuent la formation du chapeau fibreux et à long terme, contribuent à l’instabilité de la plaque. Dans cette étude, nous nous sommes intéressés à l’impact d’ARF6 sur les cellules du muscle lisse vasculaire et ses implications pathologiques dans l’athérosclérose. Les ARF sont des GTPases agissant comme interrupteurs moléculaires dans divers processus physiologiques tels que le trafic vésiculaire intracellulaire et le remodelage des lipides membranaires. ARF6 est importante pour la prolifération et la migration cellulaire des CMLV, deux phénomènes importants dans le développement de l’athérosclérose. Nous émettons donc l’hypothèse que la GTPase ARF6 est impliquée dans la progression de l’athérosclérose. En premier lieu, nous avons étudié l’effet de la GTPase dans le phénomène de l’invasion cellulaire. Dans l’athérosclérose, plusieurs facteurs environnementaux influencent l’invasion des CMLV. Nous avons voulu vérifier l’effet d’ARF6 sur l’invasion des CMLV médiée par le facteur de croissance dérivé des plaquettes (PDGF-BB) et l’angiotensine II (Ang II). Dans un modèle humain, l’invasion était diminuée en l’absence d’ARF6. Nous avons démontré que ce mécanisme résultait d’un effet d’ARF6 sur l’activité de la métalloprotéinase matricielle MMP14. En second lieu, nous avons voulu évaluer l’effet d’ARF6 dans un modèle in vivo d’athérosclérose. En utilisant un modèle accéléré d’athérosclérose inductible, nous avons inhibé ARF6 dans les cellules du muscle lisse. Après dix semaines de diète riche en gras, nous avons observé une diminution de la taille des lésions athérosclérotiques dans les souris ARF6 KO, accompagnée d’une réduction de l’expression des facteurs pro-inflammatoires tels qu’IL-6. Dans un modèle in vitro, l’absence d’ARF6 réduisait l’absorption lipidique en agissant sur l’expression des transporteurs. De plus, ARF6 régulait des voies de signalisation impliquées dans l’inflammation. En somme, nous avons démontré l’importance d’ARF6 dans la modulation pathologique des CMLV dans l’athérosclérose. Ainsi, ARF6 contribue à la pathogénicité des CMLV en modulant leur invasion cellulaire tout en jouant un rôle pro-inflammatoire. / Atherosclerosis is a chronic cardiovascular disease characterized by an accumulation of lipids, followed by the infiltration of macrophages and vascular smooth muscle cells (VSMC). VSMC are responsible for the increase of lesion size, the formation of a fibrous cap, and eventually contributing to the plaque instability. In this study, we were interested in the role of ARF6 in the vascular smooth muscle cells and its pathological implications in atherosclerosis. ARF are a family of GTPases that act as molecular switches and are involved in diverse physiological mechanisms, such as vesicular traffic and membrane lipid transformation. In VSMC, ARF6 is important for cell proliferation and migration, two processes involved in atherosclerosis. We therefore hypothesize that the GTPase ARF6 is involved in the development of atherosclerosis through its impact on VSMC. First, we studied the role of ARF6 in the mechanism of cell invasion. In atherosclerosis, multiple environmental factors affect VSMC invasion. We verified the impact of ARF6 on platelet-derived growth factor (PDGF-BB) and angiotensin II (Ang II)-mediated invasion. Using a human model, we observed a reduction of invasion in the absence of ARF6. We have demonstrated that this mechanism is due to the effect of ARF6 on the activity of the matrix metalloproteinase MMP14. Second, we wanted to verify the role of ARF6 in atherosclerosis in an in vivo model. Using an accelerated inducible atherosclerosis model, we inhibited ARF6 in smooth muscle cells. After ten weeks of high-fat diet, we observed a reduction in the size of atherosclerotic lesions in ARF6 KO mice. This reduction was accompanied by a decrease in the expression of proinflammatory factors. In our in vitro model, ARF6 depletion reduced lipid uptake by downregulating the lipidic transporter expression. Also, ARF6 was responsible to activate inflammation signaling pathways. In summary, we have demonstrated the impact of ARF6 in the pathological modulation of VSMC in atherosclerosis. Indeed, ARF6 contributes to the pathogenicity of VSMC through its ability to modulate cell invasion and induce proinflammatory actions.