Interference of doxycycline pretreatment in a model of abdominal aortic aneurysms

Mata, Karina M.; Tefé‐Silva, Cristiane; Floriano, Elaine M.; Fernandes, Cleverson Rodrigues; Rizzi, Élen; Gerlach, Raquel Fernanda; Mazzuca, M; Ramos, Simone G.

doi:10.1016/j.carpath.2014.10.004

Cited by 23 publications

(21 citation statements)

References 63 publications

(102 reference statements)

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“…In humans, MMPs have been most extensively studied [70,71]. Doxycycline, a broad spectrum MMP inhibitor, has been investigated as a potential medical approach for preventing AAA progression in animal models [72]. Recently, a randomized trial of 286 patients unexpectedly found that doxycycline administration significantly increased AAA expansion [73**].…”

Section: Potential Medical Therapy For Human Aaasmentioning

confidence: 99%

Abdominal aortic aneurysm

Davis

Rateri

Daugherty

2015

Current Opinion in Cardiology

134

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Purpose of review Abdominal aortic aneurysm (AAA) is a pathological condition of permanent dilation that portends the potentially fatal consequence of aortic rupture. This review emphasizes recent advances in mechanistic insight into aneurysm pathogenesis and potential pharmacologic therapies that are on the horizon for AAAs. Recent Findings An increasing body of evidence demonstrates that genetic factors, including 3p12.3, DAB2IP, LDLr, LRP1, MMP3, TGFβR2 and SORT1 loci, are associated with AAA development. Current human studies and animal models have shown that many leukocytes and inflammatory mediators, such as IL-1, IL-17, TGF-β and angiotensin II, are involved in the pathogenesis of AAAs. Leukocytic infiltration into aortic media leads to smooth muscle cell depletion, generation of reactive oxygen species, and extracellular matrix fragmentation. Recent preclinical investigations into pharmacological therapies for AAAs have provided intriguing insight for roles of microRNAs to regulate many pathological pathways in AAA development. Several large clinical trials are ongoing seeking to translate preclinical findings into therapeutic options. Summary Recent studies have identified many potential mechanisms involved in AAA pathogenesis that provide insight for the development of a medical treatment for this disease.

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Section: Potential Medical Therapy For Human Aaasmentioning

confidence: 99%

Abdominal aortic aneurysm

Davis

Rateri

Daugherty

2015

Current Opinion in Cardiology

134

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“…In fact, doxycycline (30 mg/Kg via gavage) was able to inhibit aneurysm formation in approximately 85% of the animals. Interestingly, its principal interference occurred through the inhibition of acute inflammatory cell afflux, avoiding the burst of neutrophils and MMP-9 responsible for most of the elastolytic activity that generated the arterial wall weakness and, consequently, aneurysm formation [4]. With doxycycline, even when aneurysms formed, they were smaller than those in the aneurysm group, suggesting that the decisive aspect was the inhibition of the acute inflammatory process and its consequences.…”

Section: Dear Dr Hanmentioning

confidence: 99%

Response to the “Letter regarding Interference of doxycycline pretreatment in a model of abdominal aortic aneurysms”

Mata

Fernandes

Tefé‐Silva

et al. 2015

Cardiovascular Pathology

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“…DOXY also exhibits direct inactivation of MMPs and expression by its antioxidant properties [36, 37]. Similarly to other studies [36, 38], herein doxycycline impaired proteolytic activity of MMP -2 and -9.…”

Section: Discussionmentioning

confidence: 61%

“…The immediate effect of DOXY in the dentin-resin interface as protease inhibitor has been recently investigated [13, 18]. Herein, a 3% DOXY primer was prepared to exert an effective MMP inactivation effect at sub-antimicrobial concentration [38]. Similar to other in vitro studies, no significant effect was observed on the TBS; but a significant decrease in enzymatic activity supports the efficacy of DOXY as MMPs inhibitor [45].…”

Section: Discussionmentioning

confidence: 92%

Experimental primers containing synthetic and natural compounds reduce enzymatic activity at the dentin–adhesive interface under cyclic loading

et al. 2016

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Objective To evaluate the effect of experimental primers (chlorhexidine, enriched mixture of proanthocyanidins and doxycycline) on the adhesive properties and gelatinolytic activity at dentin-resin interfaces of occlusal Class I restorations. Methods The inactivation of enzymes by the experimental primers was assessed by fluorescence assay and gelatin zymography. To assess the adhesive properties, occlusal Class I cavities were prepared in sound human molars, etched with phosphoric acid and restored with one of the primers and an etch-and-rinse adhesive system (Adper Single Bond Plus - 3M ESPE). After the restorative procedures, the specimens were divided into two subgroups (n = 6) consisting of storage in incubation buffer or axial cyclic loading at 50 N and 1,000,000 cycles. Then, the sectioned and sliced specimens were assigned to in situ zymography assay and microtensile bond strength (TBS) test. Results Fluorescence assay and gelatin zymography revealed that the experimental primers inactivated rMMPs. In situ zymography (2-way ANOVA, Tukey, p < 0.05) showed that cyclic loading increased the gelatinolytic activity at the resin-dentin interface and the experimental primers decreased the gelatinolytic activity at the adhesive interface. The experimental primers had no significant effects on dentin-adhesive bond strengths with or without cyclic loading (2-way ANOVA, p > 0.05). Significance The use of experimental primers impaired the enzymatic activity at the dentin-adhesive interface after cyclic loading and the activity of rMMPs. Cyclic loading did not have a significant effect on the bond strength.

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Interference of doxycycline pretreatment in a model of abdominal aortic aneurysms

Cited by 23 publications

References 63 publications

Abdominal aortic aneurysm

Abdominal aortic aneurysm

Response to the “Letter regarding Interference of doxycycline pretreatment in a model of abdominal aortic aneurysms”

Experimental primers containing synthetic and natural compounds reduce enzymatic activity at the dentin–adhesive interface under cyclic loading

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