Early degradation and serum appearance of type I collagen fragments after myocardial infarction

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1 Journal of Molecular and Cellular Cardiology 36 (04) Brief Communication Early degradation and serum appearance of type I collagen fragments after myocardial infarction Francisco Villarreal a, *, Jeffrey Omens a, Wolfgang Dillmann a, Juha Risteli b, Judy Nguyen a, James Covell a a Department of Medicine, University of California, San Diego, CA, USA b Department of Clinical Chemistry, University of Oulu, Oulu and Kuopio University Hospital, Kuopio, Finland Received 24 November 03; received in revised form December 03; accepted 7 January 04 Abstract Although extracellular matrix-degrading enzymes matrix metalloproteinases (MMPs) are activated within minutes after myocardial infarction (MI), the time course of early MI-induced type I cardiac collagen degradation has not been assessed, nor has the ability of MMP inhibitor compounds, such as doxycycline (DOX), to limit these events. The objective of this study was to assess serum biomarker evidence of myocardial type I collagen degradation early (<48 h) after coronary occlusion (CO) and determine the capacity of DOX to ameliorate its release. CO studies were performed in untreated and DOX pre-treated pigs. Treated animals received DOX at 30 mg/kg/d. Radioimmunoassays were performed for serum levels of C-terminal telopeptide of collagen type I (ICTP) fragments. ICTP groups peaked by after MI. However, in DOX-treated animals, ICTP values returned to normal by 8 h. Average serum concentrations for ICTP values from 0 to 48 h post-mi were significantly inhibited by DOX treatment. In conclusion, serum biomarker results indicate that type I collagen degradation occurs within minutes after MI and that DOX likely reduces its degradation. 03 Elsevier Ltd. All rights reserved. Keywords: Collagen; Matrix metalloproteinases; Myocardial infarction; Doxycycline; Remodeling 1. Introduction Fibrillar collagen types I and III are the major types of extracellular matrix (ECM) proteins present in the heart [1]. Type I collagen comprises about 75% of myocardial collagens. Myocardial collagens provide structural support and integrity to the heart and allow for proper pump function. Matrix metalloproteinases (MMPs) are a family of zinccontaining endoproteinases whose main substrates are ECM proteins [2]. MMPs are secreted as zymogens and require activation to generate proteolytic activity [2]. In vivo studies have documented the time-dependent activation of MMPs following myocardial infarction (MI). Activation occurs within minutes, peaking approximately 1 2 d after MI and likely reflect the activation of pre-formed MMPs [3 6]. The time course of upregulation of MMP activity suggests that a significant amount of collagen degradation occurs very early (first 48 h) after MI. * Corresponding author. Tel: ; fax: address: fvillarr@ucsd.edu (F. Villarreal). Documenting the extent of damage to the cardiac ECM after ischemic injury has been difficult and most techniques require tissue samples [7,8]. The ability to perform serial serum determinations as done with biomarkers of cardiomyocyte damage would make it possible to assess not only the presence but also the time course and magnitude of MI-induced collagen degradation [9]. Serum marker radioimmunoassays (RIAs) that measure collagen degradation and/or synthesis are readily available and have been used in the setting of cardiovascular diseases [10,11]. When soft tissue type I collagen is exposed to active MMPs, a crosslinked C-terminal telopeptide of collagen type I (ICTP) is released that eventually reaches the bloodstream [10,11]. This marker can be used to monitor type I collagen degradation. Although serum evidence for MI-mediated release of cardiac type III collagen has been reported [11], nothing is known about ischemia-mediated damage to type I collagen. MMP inhibition following MI can preserve cardiac structure and function [12 ]. Doxycycline (DOX), a tetracycline derivative, is known to exert biological effects independent of its antimicrobial activity, including acting as a broad- 03 Elsevier Ltd. All rights reserved. doi:10.10/j.yjmcc

2 598 F. Villarreal et al. / Journal of Molecular and Cellular Cardiology 36 (04) spectrum MMP inhibitor [15 ]. We recently reported that short-term pre-treatment with DOX inhibits myocardial MMP activity, ameliorates post-mi remodeling and preserves passive ventricular function in rats []. Thus the ability to monitor collagen degradation after MI may also serve to test for effects that pharmacological therapies exert on type I collagen preservation. The objectives of this study were to assess for serum biomarker evidence of the early time course of cardiac type I collagen degradation after MI and to determine the capacity of DOX pre-treatment to ameliorate MI-induced increases in this biomarker. Results indicate that type I collagen degradation can be detected in serum 15 min after MI and that DOX significantly reduced type I collagen degradation. 2. Materials and methods 2.1. DOX treatment Male pigs weighing 25 kg were used. DOX was administered orally at 30 mg/kg/d. This DOX dose effectively blocks MMP activity in models of tissue injury and healing [17,]. Pre-treatment began 48 h prior to coronary occlusion (CO) and continued until 48 h after (end of study). Groups included sham (n = 3), control untreated (n = 6) and DOXtreated (n = 5) MIs. All procedures were approved by the Institutional Animal Care and Use Committee and conform to published NIH guidelines for animal research Surgical preparation Pigs underwent a thoracotomy to place a snare around the coronary artery 1 week prior to CO. Anesthesia was induced with ketamine (100 mg/kg) and xylazine (5 mg/kg), and maintained using isoflurane positive pressure ventilation. A left thoracotomy was performed and the pericardium opened. A suture running through a plastic tube was placed around a marginal branch of the circumflex artery. The plastic snare tube was buried subcutaneously. Catheters were placed in the jugular vein for blood sampling. Animals were allowed to recover from surgery for 1 week, at which time through a small incision the snare was exteriorized and occluded (except shams) using i.v. propofol anesthesia (2.5 mg/kg). Blood (serum) samples were collected at 48 h (pre-co), 24 h, 5, 15, 30 min, 1, 2, 3, 6, 8, 24 and 48 h after CO. Electrocardiograms were monitored for evidence of MI MI size determination Forty-eight hours after CO, animals were sacrificed, hearts excised and weighed. The left ventricle (LV) was cross-sectioned into 5 6 rings, which were stained in triphenyl tetrazolium chloride (TTC). Volumetric determinations of infarct size were performed by digital tracing of TTCstained sections. Formalin-fixed LV tissue was paraffin embedded for sectioning. Border zone myocardium sections were stained using either Masson s trichrome or anti-human ICTP antibodies ICTP determinations RIA (Orion Diagnostica) antibodies to human collagen I cross-react with pig [8]. Assays were performed as previously described and ICTP values were extrapolated from standard curves as ng/ml serum [8]. Data analysis included the computation of average ICTP levels over time from 5 min to 48 h post-co (i.e. area under the curve) [9] Statistical analysis Statistical analysis was performed using a Student s t-test. Results were considered to be statistically significant at P < Results Body weights for control and DOX-treated animals averaged 22.3 ± 2.8 and 24.2 ± 3.7 kg, respectively. Heart to body weight ratios 48 h after CO were 6.4 ± 1.1 for control and 6.3 ± 0.8 for DOX. MI size as a percent of LV mass was not significantly different between control (10.0 ± 2.7%) and DOX (11.5 ± 3.7%) groups. In all animals, elevated serum levels for ICTP were observed after thoracotomy (data not shown) and likely represent surgical trauma-induced increases and may explain the failure of previous studies to observe post-mi increases [8]. ICTP levels decreased in all animals by 7 d after the initial surgery to values comparable to those previously reported for normal (non-infarcted) pigs [8]. Fig. 1a shows ICTP levels for a representative sham animal, which did not increase relative to 5 min values. Fig. 1b illustrates representative changes in ICTP levels observed in a control CO animal. CO resulted in a rapid and sustained (up to 48 h) increase in serum ICTP levels, which peaked approximately after MI. Fig. 1c exemplifies changes in ICTP levels in a CO animal pre-treated with DOX. A rapid increase in ICTP levels was observed, peaking about after CO but returning to pre-occlusion levels by 8 h. On average, ICTP levels before CO were similar for both groups (15.6 ± 2.6 ng/ml for control and ± 3.3 ng/ml for DOX animals). ICTP values in control pigs peaked at 21.5 ± 2.5 ng/ml (P < 0.05 vs. pre-co) 6.4 ± 1.8 h post-co. DOX-treated pigs ICTP values peaked at 21.5 ± 3.4 ng/ml (P = 0.13 vs. pre-co) 5.8 ± 1.8 h post-co. Fig. 2 compares increases in ICTP levels in control and DOX animals. Sustained increases over time were observed in control animals peaking approximately 8 h post-co and partially returning towards pre-co levels by 24 and 48 h. In contrast, DOX pre-treated animals demonstrated an early increase in ICTP levels and a quick return to near pre-

3 F. Villarreal et al. / Journal of Molecular and Cellular Cardiology 36 (04) occlusion occlusion 8 h 1 day A. Sham 2 h 0.5 h 8 h 1 day pre-co level 2 day B. Control 5 min 2 h 2 day C. Doxycycline pre-co level 8 h 1 day 2 day Time (h) Fig. 1. Mean ICTP levels observed in single representative sham, control and DOX-treated infarcted pigs after CO. In contrast to sham pigs, control CO pigs yielded sustained increases in ICTP levels after infarction. With DOX treatment ICTP increases were of transient nature with values returning to pre-co levels by 8 h after infarction. occlusion values. Fig. 2 compares both groups in average ICTP serum values over time (5 min to 48 h area under the curve, panel B). DOX pre-treatment significantly inhibited average ICTP serum values over time (P < 0.05) yielding comparable values to shams. Fig. 3 shows that in areas of normal myocardium, collagen fibers stained light blue by Masson s trichrome. Collagen fibers continue to be evident without a discernible difference within the border zone and necrotic areas. However, with ICTP immunostaining intense red coloring (vector red) seen ICTP Avg. Conc. (ng/ml*hr) between myofibers in normal myocardium becomes less evident towards border zone areas and disappears in necrotic areas. 4. Discussion A. B. Time (h) CTRL DOX CONTROL DOX SHAM Fig. 2. Changes observed in ICTP levels with MI. (A) Differences in serum levels observed in control (n = 6) and DOX-treated (n = 5) animals from 5 min to 48 h after CO with significant differences observed at all time points except at 6 (P = 0.4) and 48 h (P = 0.). (B) Average concentration over time (area under the curve from panel A; mean ± S.E.M.) observed from 5 min to 48 h in all groups; * indicates significant differences vs. control (P < 0.05). In the setting of MI it has been demonstrated that MMP activation occurs by 10 min after CO [3 6]. However, evidence for ECM degradation has been more difficult to obtain. Whereas studies have provided evidence of damage to collagens after MI [7] none has provided information regarding type I collagen degradation, the time course of early events and the effects of drug therapy. The analysis of changes in ICTP levels indicated that MI yielded a significant increase which became evident as early as min, peaking approximately after CO. ICTP levels in untreated CO animals remained elevated and, in contrast to the DOX-treated group, failed to return to normal by 48 h. DOX pre-treatment significantly inhibited ICTP * *

4 600 F. Villarreal et al. / Journal of Molecular and Cellular Cardiology 36 (04) Fig. 3. Immunohistochemical evidence for collagen damage with MI. Left: section stained with Masson s trichrome. Collagen fibers (light blue) can be observed both in unaffected and necrotic myocardium. Right: a comparable, alternate section stained with anti-ictp. Whereas in normal muscle red staining can be observed, in necrotic tissue the reaction is negative (no ICTP detected). These results suggest that the source of increases in serum ICTP is the ischemic/necrotic myocardium. release over time in the infarcted animals. This finding gains relevance in light of various recent reports indicating that treatment with MMP inhibitors helps preserve cardiac structure and function after MI [12 ]. We reported that in rats subjected to CO, early (0 48 h), short-term pre-treatment with DOX inhibits MMP activation, preserves LV cardiac structure and passive function 4 weeks post-mi []. In this study we postulated that short-term pre-treatment with DOX may limit the greatest damage observed in collagen matrix while not interfering with subsequent increases (>48 h) in MMP activity which may compromise the ensuing wound healing response [19]. Results from this study and from ICTP RIA measurements emphasize the importance of early events in defining post-mi outcome. However, further long-term studies are needed to determine if DOX treatment affects ventricular remodeling given that MMP activation and collagen degradation may constitute necessary components of wound healing. Indeed, studies using rat models of MI have shown that peak increases in MMP gene expression and activity can occur well beyond 48 h []. Furthermore, increases in mrna levels for tissue inhibitor of MMPs (TIMPs) were noted to occur as early as after MI peaking by 48 h []. The use of anti-ictp on tissue sections clearly identifies damage to type I collagen by failing to stain areas of necrotic myocardium. The release of the 1/4 fragment from type I collagen denatures the protein structure yielding gelatin which is susceptible to further proteolytic degradation [11]. As such, collagen type I loses its characteristic mechanical (tensile) properties. Our observations imply that in the setting of infarction a major structural component of the cardiac ECM is significantly damaged and its function is likely compromised. These observations could be complemented in future studies by biochemical measurements of collagen content. The functional implications of degradation of the cardiac ECM after MI are important and deserve further examination. Our studies were limited to permanent CO and should be extended to assess the effect of other therapeutic interventions. Furthermore, the size of the MI induced in pigs was purposefully kept uniform and small; additional studies warrant the assessment of ICTP values with varying infarct sizes. The further validation of RIA for type I collagen peptides may allow their incorporation into clinical studies to assess the effects of various therapies on ECM degradation. References [1] Caulfield JB, Borg TK. The collagen network of the heart. Lab Invest 1979;40: [2] Nagase H, Woessner Jr JF. Matrix metalloproteinases. J Biol Chem 1999;274: [3] Etoh T, Joffs C, Deschamps AM, Davis J, Dowdy K, Hendrick J, et al. Myocardial and interstitial matrix metalloproteinase activity after acute myocardial infarction in pigs. Am J Physiol 01;281:H [4] Romanic AM, Burns-Kurtis CL, Gout B, Berrebi-Bertrand I, Ohlstein EH. Matrix metalloproteinase expression in cardiac myocytes following myocardial infarction in the rabbit. Life Sci 01;68: [5] Herzog E, Gu AG, Kohmoto T, Burkhoff D, Hochman JS. Early activation of metalloproteinases after experimental myocardial infarction occurs in infarct and non-infarct zones. Cardiovasc Pathol 1998; 7: [6] Danielsen CC, Wiggers H, Andersen HR. Increased amounts of collagenase and gelatinase in porcine myocardium following ischemia and reperfusion. J Mol Cell Cardiol 1998;30: [7] Takahashi S, Barry AC, Factor SM. Collagen degradation in ischaemic rat hearts. Biochem J 1990;265: [8] Wiggers H, Klebe T, Heickendorff L, Høst NB, Danielsen CC, Baandrup U, et al. Ischemia and reperfusion of the porcine myocardium: effect on collagen. J Mol Cell Cardiol 1997;29: [9] Uusimaa P, Risteli J, Niemelä M, Lumme J, Ikäheimo M, Jounela A, et al. Collagen scar formation after acute myocardial infarction: relationships to infarct size, left ventricular function, and coronary artery patency. Circulation 1997;96: [10] Risteli L, Risteli J. Noninvasive methods for detection of organ fibrosis. Boca Raton, FL: CRC Press; [11] Weber KT. Monitoring tissue repair and fibrosis from a distance [editorial; comment]. Circulation 1997;96: [12] Rohde LE, Ducharme A, Arroyo LH, Aikawa M, Sukhova GH, Lopez- Anaya A, et al. Matrix metalloproteinase inhibition attenuates early left ventricular enlargement after experimental myocardial infarction in mice. Circulation 1999;99: [13] Lindsey ML, Gannon J, Aikawa M, Schoen FJ, Rabkin E, Lopresti- Morrow L, et al. Selective matrix metalloproteinase inhibition reduces left ventricular remodeling but does not inhibit angiogenesis after myocardial infarction. Circulation 02;105:753 8.

5 F. Villarreal et al. / Journal of Molecular and Cellular Cardiology 36 (04) [] Yarbrough WM, Mukherjee R, Escobar GP, Mingoia JT, Sample JA, Hendrick JW, et al. Selective targeting and timing of matrix metalloproteinase inhibition in post-myocardial infarction remodeling. Circulation 03;108: [15] Golub LM, Lee HM, Ryan ME, Giannobile WV, Payne J, Sorsa T. Tetracyclines inhibit connective tissue breakdown by multiple nonantimicrobial mechanisms. Adv Dent Res 1998;12: [] Villarreal FJ, Griffin M, Omens J, Dillmann W, Nguyen J, Covell J. Early short-term treatment with doxycycline modulates postinfarction left ventricular remodeling. Circulation 03;108: [17] Curci JA, Petrinec D, Liao S, Golub LM, Thompson RW. Pharmacologic suppression of experimental abdominal aortic aneurysms: a comparison of doxycycline and four chemically modified tetracyclines. J Vasc Surg 1998;28: [] Lamparter S, Slight SH, Weber KT. Doxycycline and tissue repair in rats. J Lab Clin Med 02;139: [19] Heymans S, Luttun A, Nuyens D, Theilmeier G, Creemers E, Moons L, et al. Inhibition of plasminogen activators or matrix metalloproteinases prevents cardiac rupture but impairs therapeutic angiogenesis and causes cardiac failure. Nat Med 1999;5: [] Cleutjens J, Kandala JC, Guarda E, Guntaka RV, Weber KT. Regulation of collagen degradation in the rat myocardium after infarction. J Mol Cell Cardiol 1995;27:

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